Pub Date : 2024-09-01Epub Date: 2024-07-26DOI: 10.3892/mmr.2024.13294
Yongli Hu, Bing Wang, Lie Wang, Zhenran Wang, Zhiyuan Jian, Lin Deng
Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the JC‑1 staining images in Fig. 2C were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been published elsewhere prior to the submission of this paper to Molecular Medicine Reports, or were under consideration for publication at around the same time (a small number of which have been retracted). In addition, the Snail western blot data in Fig. 3E bore a close similarity to certain of the Mfn2 data shown in Fig. 4A. In view of the fact that certain of the contentious data had already apparently been published previously, and owing to a lack of confidence in the presentation of certain of the data in this paper, the Editor of Molecular Medicine Reports has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 22: 398‑404, 2020; DOI: 10.3892/mmr.2020.11098].
{"title":"[Retracted] Mammalian STE20‑like kinase 1 regulates pancreatic cancer cell survival and migration through Mfn2‑mediated mitophagy.","authors":"Yongli Hu, Bing Wang, Lie Wang, Zhenran Wang, Zhiyuan Jian, Lin Deng","doi":"10.3892/mmr.2024.13294","DOIUrl":"10.3892/mmr.2024.13294","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the JC‑1 staining images in Fig. 2C were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been published elsewhere prior to the submission of this paper to <i>Molecular Medicine Reports</i>, or were under consideration for publication at around the same time (a small number of which have been retracted). In addition, the Snail western blot data in Fig. 3E bore a close similarity to certain of the Mfn2 data shown in Fig. 4A. In view of the fact that certain of the contentious data had already apparently been published previously, and owing to a lack of confidence in the presentation of certain of the data in this paper, the Editor of <i>Molecular Medicine Reports</i> has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 22: 398‑404, 2020; DOI: 10.3892/mmr.2020.11098].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11304385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141759865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pancreatic ductal adenocarcinoma (PDAC) is an extremely aggressive form of cancer with a low survival rate. A successful treatment strategy should not be limited to targeting cancer cells alone, but should adopt a more comprehensive approach, taking into account other influential factors. These include the extracellular matrix (ECM) and immune microenvironment, both of which are integral components of the tumor microenvironment. The present review describes the roles of pancreatic stellate cells, differentiated cancer‑associated fibroblasts and the interleukin family, either independently or in combination, in the progression of precursor lesions in pancreatic intraepithelial neoplasia and PDAC. These elements contribute to ECM deposition and immunosuppression in PDAC. Therapeutic strategies that integrate interleukin and/or stromal blockade for PDAC immunomodulation and fibrogenesis have yielded inconsistent results. A deeper comprehension of the intricate interplay between fibrosis, and immune responses could pave the way for more effective treatment targets, by elucidating the mechanisms and causes of ECM fibrosis during PDAC progression.
{"title":"Pancreatic stellate cells and the interleukin family: Linking fibrosis and immunity to pancreatic ductal adenocarcinoma (Review).","authors":"Haichao Li, Donglian Liu, Kaishu Li, Yichen Wang, Gengqiang Zhang, Ling Qi, Keping Xie","doi":"10.3892/mmr.2024.13283","DOIUrl":"10.3892/mmr.2024.13283","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is an extremely aggressive form of cancer with a low survival rate. A successful treatment strategy should not be limited to targeting cancer cells alone, but should adopt a more comprehensive approach, taking into account other influential factors. These include the extracellular matrix (ECM) and immune microenvironment, both of which are integral components of the tumor microenvironment. The present review describes the roles of pancreatic stellate cells, differentiated cancer‑associated fibroblasts and the interleukin family, either independently or in combination, in the progression of precursor lesions in pancreatic intraepithelial neoplasia and PDAC. These elements contribute to ECM deposition and immunosuppression in PDAC. Therapeutic strategies that integrate interleukin and/or stromal blockade for PDAC immunomodulation and fibrogenesis have yielded inconsistent results. A deeper comprehension of the intricate interplay between fibrosis, and immune responses could pave the way for more effective treatment targets, by elucidating the mechanisms and causes of ECM fibrosis during PDAC progression.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11258612/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-01Epub Date: 2024-07-12DOI: 10.3892/mmr.2024.13289
Peng Liu, Shuya Wang, Kaiyuan Li, Yang Yang, Yilong Man, Fengli Du, Lei Wang, Jing Tian, Guohai Su
Subsequently to the publication of the above article, the authors have realized that, in Fig. 1A, the incorrect image was uploaded to show the ultrastructure of exos isolated from plasma and examined using transmission electron microscopy (essentially, the image in question had already appeared in an article published by the same research group in Journal of Cellular and Molecular Medicine). In addition, the '+' and '-' signs for the 'Cell lysis' experiments shown underneath the gels in Fig. 1B were incorporated the wrong way around. The revised version of Fig. 1, showing the correct image in Fig. 1A and the correct labels in Fig. 1B, is shown below. Note that the errors made in assembling this figure did not have a major impact on either the results or the conclusions reported in this paper. The authors are grateful to the Editor of Molecular Medicine Reports for allowing them this opportunity to publish a corrigendum, and apologize to the readership of the Journal for any inconvenience caused. [Molecular Medicine Reports 27: 124, 2023; DOI: 10.3892/mmr.2023.13010].
{"title":"[Corrigendum] Exosomal microRNA‑4516, microRNA‑203 and SFRP1 are potential biomarkers of acute myocardial infarction.","authors":"Peng Liu, Shuya Wang, Kaiyuan Li, Yang Yang, Yilong Man, Fengli Du, Lei Wang, Jing Tian, Guohai Su","doi":"10.3892/mmr.2024.13289","DOIUrl":"10.3892/mmr.2024.13289","url":null,"abstract":"<p><p>Subsequently to the publication of the above article, the authors have realized that, in Fig. 1A, the incorrect image was uploaded to show the ultrastructure of exos isolated from plasma and examined using transmission electron microscopy (essentially, the image in question had already appeared in an article published by the same research group in <i>Journal of Cellular and Molecular Medicine</i>). In addition, the '+' and '-' signs for the 'Cell lysis' experiments shown underneath the gels in Fig. 1B were incorporated the wrong way around. The revised version of Fig. 1, showing the correct image in Fig. 1A and the correct labels in Fig. 1B, is shown below. Note that the errors made in assembling this figure did not have a major impact on either the results or the conclusions reported in this paper. The authors are grateful to the Editor of <i>Molecular Medicine Reports</i> for allowing them this opportunity to publish a corrigendum, and apologize to the readership of the Journal for any inconvenience caused. [Molecular Medicine Reports 27: 124, 2023; DOI: 10.3892/mmr.2023.13010].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11267248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Following the publication of the above article, the authors realized that, in Fig. 1D on p. 7363, the data panel selected for the '0.5 mM Succinate' group was duplicated in Fig. 1B (Control) in another article of theirs published in FASEB J ("α‑Ketoglutarate prevents skeletal muscle protein degradation and muscle atrophy through PHD3/ADRB2 pathway": doi: 10.1096/fj.201700670R) due to the fact that they had inadvertently confused the layout of the two figures. The authors apologize for this error. Secondly, in terms of the quantification of the blots shown in Fig. 2A, β‑actin was not in fact used as a loading control; the phosphoproteins were normalized against the levels of the relative total protein, and the layout of Fig. 2A has been revised to reflect this (note that the the figure legend for Fig. 2 has also been revised: The last sentence no longer reads, "β‑actin was used as a loading control."). The revised versions of Figs. 1 and 2 are shown on the next page. Note that these errors did not affect the results or the main conclusions reported in the study, and no corrections were required either to the descriptions in the text or to the histograms shown in these figures. All the authors approve of the publication of this corrigendum, and the authors are grateful to the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this. The authors regret their oversight in allowing these errors to be included in the paper, and apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 16: 7361‑7366, 2017; DOI: 10.3892/mmr.2017.7554].
{"title":"[Corrigendum] Succinate promotes skeletal muscle protein synthesis via Erk1/2 signaling pathway.","authors":"Yexian Yuan, Yaqiong Xu, Jingren Xu, Bingqing Liang, Xingcai Cai, Canjun Zhu, Lina Wang, Songbo Wang, Xiaotong Zhu, Ping Gao, Xiuqi Wang, Yongliang Zhang, Qingyan Jiang, Gang Shu","doi":"10.3892/mmr.2024.13293","DOIUrl":"10.3892/mmr.2024.13293","url":null,"abstract":"<p><p>Following the publication of the above article, the authors realized that, in Fig. 1D on p. 7363, the data panel selected for the '0.5 mM Succinate' group was duplicated in Fig. 1B (Control) in another article of theirs published in <i>FASEB J</i> (\"α‑Ketoglutarate prevents skeletal muscle protein degradation and muscle atrophy through PHD3/ADRB2 pathway\": doi: 10.1096/fj.201700670R) due to the fact that they had inadvertently confused the layout of the two figures. The authors apologize for this error. Secondly, in terms of the quantification of the blots shown in Fig. 2A, β‑actin was not in fact used as a loading control; the phosphoproteins were normalized against the levels of the relative total protein, and the layout of Fig. 2A has been revised to reflect this (note that the the figure legend for Fig. 2 has also been revised: The last sentence no longer reads, \"β‑actin was used as a loading control.\"). The revised versions of Figs. 1 and 2 are shown on the next page. Note that these errors did not affect the results or the main conclusions reported in the study, and no corrections were required either to the descriptions in the text or to the histograms shown in these figures. All the authors approve of the publication of this corrigendum, and the authors are grateful to the Editor of <i>Molecular Medicine Reports</i> for allowing them the opportunity to publish this. The authors regret their oversight in allowing these errors to be included in the paper, and apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 16: 7361‑7366, 2017; DOI: 10.3892/mmr.2017.7554].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11284843/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141723981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-01Epub Date: 2024-07-12DOI: 10.3892/mmr.2024.13287
Ruxia Han, Xueying Li, Xinfu Gao, Guangyao Lv
Cancer incidence is increasing globally, presenting a growing public health challenge. While anticancer drugs are crucial in treatment, their limitations, including poor targeting ability and high toxicity, hinder effectiveness and patient safety, requiring relentless scientific research and technological advancements to develop safer and more effective therapeutics. Cinnamaldehyde (CA), an active compound derived from the natural plant cinnamon, has garnered attention in pharmacological research due to its diverse therapeutic applications. CA has potential in treating a wide array of conditions, including cardiovascular diseases, diabetes, inflammatory disorders and various forms of cancer. The present review comprehensively summarizes the physicochemical and pharmacokinetic profiles of CA, and delves into the latest advancements in elucidating its potential mechanisms and targets across various cancer types. CA and its derivatives have antitumor effects, which encompass inhibiting cell proliferation, arresting the cell cycle, inducing apoptosis, limiting cell migration and invasion, and suppressing angiogenesis. Additionally, the present review explores targeted formulations of CA, laying a scientific foundation for further exploration of its implications in cancer prevention and treatment strategies.
癌症发病率在全球范围内不断上升,给公共卫生带来了日益严峻的挑战。抗癌药物是治疗癌症的关键,但它们的局限性,包括靶向能力差和毒性大,阻碍了治疗效果和患者安全,需要不懈的科学研究和技术进步来开发更安全、更有效的疗法。肉桂醛(Cinnamaldehyde,CA)是从天然植物肉桂中提取的一种活性化合物,因其多种多样的治疗应用而在药理学研究中备受关注。肉桂醛具有治疗多种疾病的潜力,包括心血管疾病、糖尿病、炎症性疾病和各种癌症。本综述全面总结了 CA 的理化和药代动力学特征,并深入探讨了阐明其潜在机制和各种癌症类型靶点的最新进展。CA 及其衍生物具有抗肿瘤作用,包括抑制细胞增殖、阻止细胞周期、诱导细胞凋亡、限制细胞迁移和侵袭以及抑制血管生成。此外,本综述还探讨了 CA 的靶向制剂,为进一步探索其在癌症预防和治疗策略中的意义奠定了科学基础。
{"title":"Cinnamaldehyde: Pharmacokinetics, anticancer properties and therapeutic potential (Review).","authors":"Ruxia Han, Xueying Li, Xinfu Gao, Guangyao Lv","doi":"10.3892/mmr.2024.13287","DOIUrl":"10.3892/mmr.2024.13287","url":null,"abstract":"<p><p>Cancer incidence is increasing globally, presenting a growing public health challenge. While anticancer drugs are crucial in treatment, their limitations, including poor targeting ability and high toxicity, hinder effectiveness and patient safety, requiring relentless scientific research and technological advancements to develop safer and more effective therapeutics. Cinnamaldehyde (CA), an active compound derived from the natural plant cinnamon, has garnered attention in pharmacological research due to its diverse therapeutic applications. CA has potential in treating a wide array of conditions, including cardiovascular diseases, diabetes, inflammatory disorders and various forms of cancer. The present review comprehensively summarizes the physicochemical and pharmacokinetic profiles of CA, and delves into the latest advancements in elucidating its potential mechanisms and targets across various cancer types. CA and its derivatives have antitumor effects, which encompass inhibiting cell proliferation, arresting the cell cycle, inducing apoptosis, limiting cell migration and invasion, and suppressing angiogenesis. Additionally, the present review explores targeted formulations of CA, laying a scientific foundation for further exploration of its implications in cancer prevention and treatment strategies.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11267250/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-01Epub Date: 2024-07-12DOI: 10.3892/mmr.2024.13286
Cen Jin, Sijian Liao, Guoliang Lu, Bill D Geng, Zi Ye, Jianwei Xu, Guo Ge, Dan Yang
The treatment of patients with metastatic prostate cancer (PCa) is considered to be a long‑standing challenge. Conventional treatments for metastatic PCa, such as radical prostatectomy, radiotherapy and androgen receptor‑targeted therapy, induce senescence of PCa cells to a certain extent. While senescent cells can impede tumor growth through the restriction of cell proliferation and increasing immune clearance, the senescent microenvironment may concurrently stimulate the secretion of a senescence‑associated secretory phenotype and diminish immune cell function, which promotes PCa recurrence and metastasis. Resistance to established therapies is the primary obstacle in treating metastatic PCa as it can lead to progression towards an incurable state of disease. Therefore, understanding the molecular mechanisms that underly the progression of PCa is crucial for the development of novel therapeutic approaches. The present study reviews the phenomenon of treatment‑induced senescence in PCa, the dual role of senescence in PCa treatments and the mechanisms through which senescence promotes PCa metastasis. Furthermore, the present review discusses potential therapeutic strategies to target the aforementioned processes with the aim of providing insights into the evolving therapeutic landscape for the treatment of metastatic PCa.
{"title":"Cellular senescence in metastatic prostate cancer: A therapeutic opportunity or challenge (Review).","authors":"Cen Jin, Sijian Liao, Guoliang Lu, Bill D Geng, Zi Ye, Jianwei Xu, Guo Ge, Dan Yang","doi":"10.3892/mmr.2024.13286","DOIUrl":"10.3892/mmr.2024.13286","url":null,"abstract":"<p><p>The treatment of patients with metastatic prostate cancer (PCa) is considered to be a long‑standing challenge. Conventional treatments for metastatic PCa, such as radical prostatectomy, radiotherapy and androgen receptor‑targeted therapy, induce senescence of PCa cells to a certain extent. While senescent cells can impede tumor growth through the restriction of cell proliferation and increasing immune clearance, the senescent microenvironment may concurrently stimulate the secretion of a senescence‑associated secretory phenotype and diminish immune cell function, which promotes PCa recurrence and metastasis. Resistance to established therapies is the primary obstacle in treating metastatic PCa as it can lead to progression towards an incurable state of disease. Therefore, understanding the molecular mechanisms that underly the progression of PCa is crucial for the development of novel therapeutic approaches. The present study reviews the phenomenon of treatment‑induced senescence in PCa, the dual role of senescence in PCa treatments and the mechanisms through which senescence promotes PCa metastasis. Furthermore, the present review discusses potential therapeutic strategies to target the aforementioned processes with the aim of providing insights into the evolving therapeutic landscape for the treatment of metastatic PCa.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11258599/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-01Epub Date: 2024-07-26DOI: 10.3892/mmr.2024.13295
Xinjian Zhou, Minpeng Wang, Menghan Sun, Nana Yao
Sepsis is a life‑threatening multiple organ failure disease caused by an uncontrolled inflammatory response and can progress to acute lung injury (ALI). Heat‑shock protein B8 (HSPB8) serves a cytoprotective role in multiple types of diseases; however, to the best of our knowledge, the regulatory role of HSPB8 in sepsis‑induced ALI remains unclear. A549 human alveolar type II epithelial cells were treated with lipopolysaccharide (LPS) for 24 h to simulate a sepsis‑induced ALI model. Cell transfection was performed to overexpress HSPB8, and cells were treated with mitochondrial division inhibitor‑1 (Mdivi‑1) for 2 h before LPS induction to assess the underlying mechanism. Protein expression was evaluated using western blotting and an immunofluorescence assay. Cytokines were examined using ELISA assay kits and antioxidant enzymes were examined using their detection kits. Cell apoptosis was detected using flow cytometry. The mitochondrial membrane potential was detected by JC‑1 staining. HSPB8 was upregulated in A549 cells treated with LPS and HSPB8 overexpression attenuated LPS‑induced inflammatory cytokine levels, oxidative stress and apoptosis in A549 cells. LPS inhibited mitophagy and reduced the mitochondrial membrane potential in A549 cells, which was partly inhibited by HSPB8 overexpression. Furthermore, Mdivi‑1 decreased the inhibitory effect of HSPB8 on the inflammatory response, oxidative stress and apoptosis in LPS‑treated A549 cells. In conclusion, HSPB8 overexpression attenuated the LPS‑mediated inflammatory response, oxidative stress and apoptosis in A549 cells by promoting mitophagy, indicating HSPB8 as a potential therapeutic target in sepsis‑induced ALI.
{"title":"HSPB8 attenuates lipopolysaccharide‑mediated acute lung injury in A549 cells by activating mitophagy.","authors":"Xinjian Zhou, Minpeng Wang, Menghan Sun, Nana Yao","doi":"10.3892/mmr.2024.13295","DOIUrl":"10.3892/mmr.2024.13295","url":null,"abstract":"<p><p>Sepsis is a life‑threatening multiple organ failure disease caused by an uncontrolled inflammatory response and can progress to acute lung injury (ALI). Heat‑shock protein B8 (HSPB8) serves a cytoprotective role in multiple types of diseases; however, to the best of our knowledge, the regulatory role of HSPB8 in sepsis‑induced ALI remains unclear. A549 human alveolar type II epithelial cells were treated with lipopolysaccharide (LPS) for 24 h to simulate a sepsis‑induced ALI model. Cell transfection was performed to overexpress HSPB8, and cells were treated with mitochondrial division inhibitor‑1 (Mdivi‑1) for 2 h before LPS induction to assess the underlying mechanism. Protein expression was evaluated using western blotting and an immunofluorescence assay. Cytokines were examined using ELISA assay kits and antioxidant enzymes were examined using their detection kits. Cell apoptosis was detected using flow cytometry. The mitochondrial membrane potential was detected by JC‑1 staining. HSPB8 was upregulated in A549 cells treated with LPS and HSPB8 overexpression attenuated LPS‑induced inflammatory cytokine levels, oxidative stress and apoptosis in A549 cells. LPS inhibited mitophagy and reduced the mitochondrial membrane potential in A549 cells, which was partly inhibited by HSPB8 overexpression. Furthermore, Mdivi‑1 decreased the inhibitory effect of HSPB8 on the inflammatory response, oxidative stress and apoptosis in LPS‑treated A549 cells. In conclusion, HSPB8 overexpression attenuated the LPS‑mediated inflammatory response, oxidative stress and apoptosis in A549 cells by promoting mitophagy, indicating HSPB8 as a potential therapeutic target in sepsis‑induced ALI.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11294906/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141759866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-01Epub Date: 2024-07-19DOI: 10.3892/mmr.2024.13291
Jianhua Luo, Yan Jin, Mengyuan Li, Liyang Dong
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the colony formation assay data shown in Fig. 2F, the tumor images in Fig. 3A, the "NC" experiment for the Ki67 immunohistochemical staining experiment shown in Fig. 3E and the migration assay data in Fig. 4D were strikingly similar to data appearing in different form in other papers by different authors at different research institutes that had either already been published, or were under consideration for publication at around the same time. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 23: 385, 2021; DOI: 10.3892/mmr.2021.12024].
{"title":"[Retracted] Tumor suppressor miR‑613 induces cisplatin sensitivity in non‑small cell lung cancer cells by targeting GJA1.","authors":"Jianhua Luo, Yan Jin, Mengyuan Li, Liyang Dong","doi":"10.3892/mmr.2024.13291","DOIUrl":"10.3892/mmr.2024.13291","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the colony formation assay data shown in Fig. 2F, the tumor images in Fig. 3A, the \"NC\" experiment for the Ki67 immunohistochemical staining experiment shown in Fig. 3E and the migration assay data in Fig. 4D were strikingly similar to data appearing in different form in other papers by different authors at different research institutes that had either already been published, or were under consideration for publication at around the same time. Owing to the fact that the contentious data in the above article had already been published prior to its submission to <i>Molecular Medicine Reports</i>, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 23: 385, 2021; DOI: 10.3892/mmr.2021.12024].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11267435/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141723982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-01Epub Date: 2024-07-04DOI: 10.3892/mmr.2024.13274
Yong Su, Qiaoling Zhou, Qiong Wu, Yijie Ding, Meijie Jiang, Xiaoyu Zhang, Jia Wang, Xinming Wang, Chaoliang Ge
Cirrhosis impairs macrophage function and disrupts bile acid homeostasis. Although bile acids affect macrophage function in patients with sepsis, whether and how the bile acid profile is changed by infection in patients with cirrhosis to modulate macrophage function remains unclear. The present study aimed to investigate the changes in the bile acid profile of patients with cirrhosis and infection and their effects on macrophage function. Serum was collected from 20 healthy subjects, 18 patients with cirrhosis and 39 patients with cirrhosis and infection. Bile acid profiles were detected using high‑performance liquid chromatography‑triple time‑of‑flight mass spectrometer. The association between bile acid changes and infection was analysed using receiver operating characteristic (ROC) curves. Infection‑altered bile acids were used in combination with lipopolysaccharides (LPS) to stimulate RAW264.7/THP‑1 cells in vitro. The migratory capacity was evaluated using wound healing and Transwell migration assays. The expression of Arg‑1, iNOS, IκBα, phosphorylated (p‑)IκBα and p65 was examined with western blotting and immunofluorescence, Tnfα, Il1b and Il6 mRNA was examined with RT‑qPCR, and CD86, CD163 and phagocytosis was measured with flow cytometry. The ROC curves showed that decreased hyodeoxycholic acid (HDCA) and deoxycholic acid (DCA) levels were associated with infection. HDCA or DCA combined with LPS enhanced the phagocytic and migratory ability of macrophages, accompanied by upregulation of iNOS and CD86 protein expression as well as Tnfα, Il1b, and Il6 mRNA expression. However, neither HDCA nor DCA alone showed an effect on these phenotypes. In addition, DCA and HDCA acted synergistically with LPS to increase the expression of p‑IκBα and the intranuclear migration of p65. Infection changed the bile acid profile in patients with cirrhosis, among which the reduction of DCA and HDCA associated most strongly with infection. HDCA and DCA enhanced the sensitivity of macrophage function loss to LPS stimulation. These findings suggested a potential role for monitoring the bile acid profile that could help manage patients with cirrhosis and infection.
{"title":"Infection‑associated bile acid disturbance contributes to macrophage activation in patients with cirrhosis.","authors":"Yong Su, Qiaoling Zhou, Qiong Wu, Yijie Ding, Meijie Jiang, Xiaoyu Zhang, Jia Wang, Xinming Wang, Chaoliang Ge","doi":"10.3892/mmr.2024.13274","DOIUrl":"10.3892/mmr.2024.13274","url":null,"abstract":"<p><p>Cirrhosis impairs macrophage function and disrupts bile acid homeostasis. Although bile acids affect macrophage function in patients with sepsis, whether and how the bile acid profile is changed by infection in patients with cirrhosis to modulate macrophage function remains unclear. The present study aimed to investigate the changes in the bile acid profile of patients with cirrhosis and infection and their effects on macrophage function. Serum was collected from 20 healthy subjects, 18 patients with cirrhosis and 39 patients with cirrhosis and infection. Bile acid profiles were detected using high‑performance liquid chromatography‑triple time‑of‑flight mass spectrometer. The association between bile acid changes and infection was analysed using receiver operating characteristic (ROC) curves. Infection‑altered bile acids were used in combination with lipopolysaccharides (LPS) to stimulate RAW264.7/THP‑1 cells <i>in vitro</i>. The migratory capacity was evaluated using wound healing and Transwell migration assays. The expression of Arg‑1, iNOS, IκBα, phosphorylated (p‑)IκBα and p65 was examined with western blotting and immunofluorescence, <i>Tnfα</i>, <i>Il1b</i> and <i>Il6</i> mRNA was examined with RT‑qPCR, and CD86, CD163 and phagocytosis was measured with flow cytometry. The ROC curves showed that decreased hyodeoxycholic acid (HDCA) and deoxycholic acid (DCA) levels were associated with infection. HDCA or DCA combined with LPS enhanced the phagocytic and migratory ability of macrophages, accompanied by upregulation of iNOS and CD86 protein expression as well as <i>Tnfα</i>, <i>Il1b</i>, and <i>Il6</i> mRNA expression. However, neither HDCA nor DCA alone showed an effect on these phenotypes. In addition, DCA and HDCA acted synergistically with LPS to increase the expression of p‑IκBα and the intranuclear migration of p65. Infection changed the bile acid profile in patients with cirrhosis, among which the reduction of DCA and HDCA associated most strongly with infection. HDCA and DCA enhanced the sensitivity of macrophage function loss to LPS stimulation. These findings suggested a potential role for monitoring the bile acid profile that could help manage patients with cirrhosis and infection.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11234163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141498452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Viral infections in the respiratory tract are common, and, in recent years, severe acute respiratory syndrome coronavirus 2 outbreaks have highlighted the effect of viral infections on antiviral innate immune and inflammatory reactions. Specific treatments for numerous viral respiratory infections have not yet been established and they are mainly treated symptomatically. Therefore, understanding the details of the innate immune system underlying the airway epithelium is crucial for the development of new therapies. The present study aimed to investigate the function and expression of interferon (IFN)‑stimulated gene (ISG)60 in non‑cancerous bronchial epithelial BEAS‑2B cells exposed to a Toll‑like receptor 3 agonist. BEAS‑2B cells were treated with a synthetic TLR3 ligand, polyinosinic‑polycytidylic acid (poly IC). The mRNA and protein expression levels of ISG60 were analyzed using reverse transcription‑quantitative PCR and western blotting, respectively. The levels of C‑X‑C motif chemokine ligand 10 (CXCL10) were examined using an enzyme‑linked immunosorbent assay, and the effects of knockdown of IFN‑β, ISG60 and ISG56 were examined using specific small interfering RNAs. Notably, ISG60 expression was increased in proportion to poly IC concentration, and recombinant human IFN‑β also induced ISG60 expression. By contrast, knockdown of IFN‑β and ISG56 decreased ISG60 expression, and ISG60 knockdown reduced CXCL10 and ISG56 expression. These findings suggested that ISG60 is partly implicated in CXCL10 expression and that ISG60 may serve a role in the innate immune response of bronchial epithelial cells. The present study highlights ISG60 as a potential target for new therapeutic strategies against viral infections in the airway.
{"title":"Expression of ISG60 is induced by TLR3 signaling in BEAS‑2B bronchial epithelial cells: Possible involvement in CXCL10 expression.","authors":"Yusuke Tanaka, Tadaatsu Imaizumi, Yuri Kobori, Mayuki Tachizaki, Toshihiro Shiratori, Masaki Dobashi, Mami Sato, Shogo Kawaguchi, Kazuhiko Seya, Sadatomo Tasaka","doi":"10.3892/mmr.2024.13276","DOIUrl":"10.3892/mmr.2024.13276","url":null,"abstract":"<p><p>Viral infections in the respiratory tract are common, and, in recent years, severe acute respiratory syndrome coronavirus 2 outbreaks have highlighted the effect of viral infections on antiviral innate immune and inflammatory reactions. Specific treatments for numerous viral respiratory infections have not yet been established and they are mainly treated symptomatically. Therefore, understanding the details of the innate immune system underlying the airway epithelium is crucial for the development of new therapies. The present study aimed to investigate the function and expression of interferon (IFN)‑stimulated gene (ISG)60 in non‑cancerous bronchial epithelial BEAS‑2B cells exposed to a Toll‑like receptor 3 agonist. BEAS‑2B cells were treated with a synthetic TLR3 ligand, polyinosinic‑polycytidylic acid (poly IC). The mRNA and protein expression levels of ISG60 were analyzed using reverse transcription‑quantitative PCR and western blotting, respectively. The levels of C‑X‑C motif chemokine ligand 10 (CXCL10) were examined using an enzyme‑linked immunosorbent assay, and the effects of knockdown of IFN‑β, ISG60 and ISG56 were examined using specific small interfering RNAs. Notably, ISG60 expression was increased in proportion to poly IC concentration, and recombinant human IFN‑β also induced ISG60 expression. By contrast, knockdown of IFN‑β and ISG56 decreased ISG60 expression, and ISG60 knockdown reduced CXCL10 and ISG56 expression. These findings suggested that ISG60 is partly implicated in CXCL10 expression and that ISG60 may serve a role in the innate immune response of bronchial epithelial cells. The present study highlights ISG60 as a potential target for new therapeutic strategies against viral infections in the airway.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141498505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}