Molecular and Cellular Probes最新文献

Clinical value of microRNA-4449 of non-small cell lung cancer patients undergoing thoracic paravertebral block thoracotomy

IF 2.3 3区生物学 Q3 BIOCHEMICAL RESEARCH METHODS

Molecular and Cellular Probes

Pub Date : 2025-03-01 DOI: 10.1016/j.mcp.2025.102020

Yu Sun , Jiantao Zhang , Licai Zhang , Liquan Qiu , Huayi Zhang

Objective

The aim of this study was to investigate the clinical significance of microRNA-4449 (miR-4449) in patients attacked by non-small cell lung cancer (NSCLC) undergoing thoracic paravertebral block (TPVB) thoracotomy.

Methods

A total of 122 patients diagnosed with NSCLC and 101 healthy individuals were recruited in this case-control study. Quantitative real-time polymerase reaction time (qRT-PCR) assay was applied to quantify the serum levels of miR-4449 in all participants. To assess the diagnostic potential of miR-4449, receiver operating characteristic (ROC) curves were constructed. Additionally, the prognostic value of miR-4449 was evaluated using Kaplan-Meier method and Cox regression analyses. The possible target genes and related proteins of miR-4449 were predicted via bioinformatics analysis.

Results

MiR-4449 expression was notably reduced in NSCLC patients relative to healthy volunteers (P < 0.001), with the area under the curve (AUC) reaching 0.952, demonstrating its ability to effectively differentiate between NSCLC patients and healthy individuals. Serum levels of miR-4449 were negatively in relation to tumor node metastasis stage and lymph node metastasis (P < 0.05). Moreover, a significant increase in miR-4449 expression was observed in patients following TPVB thoracotomy, as compared to pre-operative levels (P < 0.001). The AUC of 0.884 further highlighted its potential to distinguish between the effective group and the invalid group. Notably, patients expressing high levels of miR-4449 exhibited improved overall survival (P < 0.001), and miR-4449 (P < 0.001, HR = 2.290, 95 % = 1.450–3.615) was identified as an independently prognostic predictor for NSCLC. Bioinformatics analysis of miR-4999 target genes revealed key tumor-associated pathways and proteins, offering valuable insights into its molecular mechanisms in NSCLC.

Conclusion

Serum levels of miR-4449 were significantly decreased in patients with NSCLC and exhibited a correlation with the severity of the tumor. Furthermore, miR-4449 emerged as a potential prognostic biomarker, offering valuable insight into the clinical outcome for NSCLC undergoing TPVB thoracotomy.

研究目的本研究旨在探讨接受胸椎旁阻滞（TPVB）开胸手术的非小细胞肺癌（NSCLC）患者体内microRNA-4449（miR-4449）的临床意义：这项病例对照研究共招募了 122 名确诊为 NSCLC 的患者和 101 名健康人。采用实时定量聚合酶反应时间（qRT-PCR）测定所有参与者血清中的 miR-4449 水平。为了评估 miR-4449 的诊断潜力，研究人员绘制了接收者操作特征曲线（ROC）。此外，还使用 Kaplan-Meier 法和 Cox 回归分析评估了 miR-4449 的预后价值。通过生物信息学分析预测了miR-4449可能的靶基因和相关蛋白：结果：与健康志愿者相比，NSCLC 患者的 miR-4449 表达明显降低（PC结论：血清中 miR-4449 的水平在 NSCLC 患者中明显降低：NSCLC患者血清中的miR-4449水平明显下降，并与疾病的严重程度相关。此外，miR-4449还是一种潜在的预后生物标志物，为了解接受TPVB开胸手术的NSCLC患者的临床预后提供了有价值的信息。

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引用次数: 0

Serum exosomal miR-454-3p contributes to malignant progression of lung cancer by inhibiting HHEX

IF 2.3 3区生物学 Q3 BIOCHEMICAL RESEARCH METHODS

Molecular and Cellular Probes

Pub Date : 2025-02-16 DOI: 10.1016/j.mcp.2025.102019

Gangqin Hu, Peng Cai, Jingjing Li, Liuyang Yu, Bolin Zhao, Guiming Chen

Background

Lung cancer is a common cancer. Exosomes are emerging mediators of intercellular communication, and miRNAs serve a crucial position in cancer progression. This project intends to discover whether exosomal miR-454-3p affects tumor progression and its underlying mechanisms.

Methods

Exosomes were isolated utilizing ultracentrifugation. The exosomal biomarkers level was monitored by western blot (WB). The miR-454-3p levels were assessed by quantitative reverse transcription polymerase chain reaction (qRT-PCR), and HHEX expression were detected by qRT-PCR and WB. Cell growth and metastasis were detected through CCK-8, colony formation assay and transwell. Meanwhile, the dual luciferase reporter system and immunoprecipitation (RIP) assay was applied to clarify the interactions between miR-454-3p and HHEX.

Results

We successfully isolated serum exosomes from NSCLC patients. Then, our team discovered that miR-454-3p was elevated in serum-derived exosomes from NSCLC patients. Functional analysis disclosed that exosomes accelerated NSCLC cell proliferation and metastasis. Silencing of exosomal miR-454-3p hindered NSCLC cell proliferation and metastasis. Subsequently, the starbase database declared that miR-454-3p was interacted with HHEX. HHEX overexpression reversed the promotion of NSCLC cell proliferation and metastasis by exosomal miR-454-3p.

Conclusions

Exosomal miR-454-3p enhanced the progression of NSCLC cells through HHEX. miR-454-3p may be a therapeutic target for NSCLC.

{"title":"Serum exosomal miR-454-3p contributes to malignant progression of lung cancer by inhibiting HHEX","authors":"Gangqin Hu, Peng Cai, Jingjing Li, Liuyang Yu, Bolin Zhao, Guiming Chen","doi":"10.1016/j.mcp.2025.102019","DOIUrl":"10.1016/j.mcp.2025.102019","url":null,"abstract":"<div><h3>Background</h3><div>Lung cancer is a common cancer. Exosomes are emerging mediators of intercellular communication, and miRNAs serve a crucial position in cancer progression. This project intends to discover whether exosomal miR-454-3p affects tumor progression and its underlying mechanisms.</div></div><div><h3>Methods</h3><div>Exosomes were isolated utilizing ultracentrifugation. The exosomal biomarkers level was monitored by western blot (WB). The miR-454-3p levels were assessed by quantitative reverse transcription polymerase chain reaction (qRT-PCR), and HHEX expression were detected by qRT-PCR and WB. Cell growth and metastasis were detected through CCK-8, colony formation assay and transwell. Meanwhile, the dual luciferase reporter system and immunoprecipitation (RIP) assay was applied to clarify the interactions between miR-454-3p and HHEX.</div></div><div><h3>Results</h3><div>We successfully isolated serum exosomes from NSCLC patients. Then, our team discovered that miR-454-3p was elevated in serum-derived exosomes from NSCLC patients. Functional analysis disclosed that exosomes accelerated NSCLC cell proliferation and metastasis. Silencing of exosomal miR-454-3p hindered NSCLC cell proliferation and metastasis. Subsequently, the starbase database declared that miR-454-3p was interacted with HHEX. HHEX overexpression reversed the promotion of NSCLC cell proliferation and metastasis by exosomal miR-454-3p.</div></div><div><h3>Conclusions</h3><div>Exosomal miR-454-3p enhanced the progression of NSCLC cells through HHEX. miR-454-3p may be a therapeutic target for NSCLC.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"80 ","pages":"Article 102019"},"PeriodicalIF":2.3,"publicationDate":"2025-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143392333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of APOA1-AS in colorectal cancer: Investigating its association with malignant biological behaviors APOA1-AS 在结直肠癌中的作用：研究其与恶性生物学行为的关系

IF 2.3 3区生物学 Q3 BIOCHEMICAL RESEARCH METHODS

Molecular and Cellular Probes

Pub Date : 2025-02-16 DOI: 10.1016/j.mcp.2025.102017

Gang Liu , Qin Zhao , Yan Li , Dongmei Zhu , Hong Peng

Purpose

Colorectal cancer (CRC) is a common malignant tumor associated with high morbidity and mortality. Long non-coding RNAs (lncRNAs) play crucial roles in cancer development and progression. This study aimed to explore the role of lncRNA APOA1-AS in colorectal cancer and elucidate its underlying mechanisms.

Methods

Clinical samples were collected, and high-throughput sequencing was performed to identify differentially expressed lncRNAs in colorectal cancer. Among these, the key lncRNA APOA1-AS was selected for further investigation. The expression of APOA1-AS in colorectal cancer tissues and cells was evaluated. The effects of APOA1-AS on cell proliferation, migration, invasion, and apoptosis were assessed through knockdown and overexpression of APOA1-AS in SW620 and RKO cells. Additionally, the relationship between APOA1-AS and the malignant biological behaviors of colorectal cancer cells was also investigated. Furthermore, the involvement of APOA1-AS in glucose metabolism reprogramming and the cGMP-PKG signaling pathway was analyzed.

Results

A total of 2985 differentially expressed lncRNAs were identified in colorectal cancer, including APOA1-AS, which showed the most significant upregulation. APOA1-AS expression was significantly higher in colorectal cancer tissues compared to normal tissues. Overexpression of APOA1-AS promoted cell proliferation, migration, and invasion while inhibiting apoptosis in SW620 and RKO cells. Furthermore, APOA1-AS was found to regulate glucose metabolism reprogramming, enhance tumor malignant biological behaviors and facilitate tumor cell drug resistance through the cGMP-PKG signaling pathway.

Conclusion

Our study demonstrates that APOA1-AS is a potential key regulator in colorectal cancer development and progression. It functions via glucose metabolism reprogramming and the cGMP-PKG signaling pathway, offering a novel therapeutic target for colorectal cancer.

{"title":"The role of APOA1-AS in colorectal cancer: Investigating its association with malignant biological behaviors","authors":"Gang Liu , Qin Zhao , Yan Li , Dongmei Zhu , Hong Peng","doi":"10.1016/j.mcp.2025.102017","DOIUrl":"10.1016/j.mcp.2025.102017","url":null,"abstract":"<div><h3>Purpose</h3><div>Colorectal cancer (CRC) is a common malignant tumor associated with high morbidity and mortality. Long non-coding RNAs (lncRNAs) play crucial roles in cancer development and progression. This study aimed to explore the role of lncRNA APOA1-AS in colorectal cancer and elucidate its underlying mechanisms.</div></div><div><h3>Methods</h3><div>Clinical samples were collected, and high-throughput sequencing was performed to identify differentially expressed lncRNAs in colorectal cancer. Among these, the key lncRNA APOA1-AS was selected for further investigation. The expression of APOA1-AS in colorectal cancer tissues and cells was evaluated. The effects of APOA1-AS on cell proliferation, migration, invasion, and apoptosis were assessed through knockdown and overexpression of APOA1-AS in SW620 and RKO cells. Additionally, the relationship between APOA1-AS and the malignant biological behaviors of colorectal cancer cells was also investigated. Furthermore, the involvement of APOA1-AS in glucose metabolism reprogramming and the cGMP-PKG signaling pathway was analyzed.</div></div><div><h3>Results</h3><div>A total of 2985 differentially expressed lncRNAs were identified in colorectal cancer, including APOA1-AS, which showed the most significant upregulation. APOA1-AS expression was significantly higher in colorectal cancer tissues compared to normal tissues. Overexpression of APOA1-AS promoted cell proliferation, migration, and invasion while inhibiting apoptosis in SW620 and RKO cells. Furthermore, APOA1-AS was found to regulate glucose metabolism reprogramming, enhance tumor malignant biological behaviors and facilitate tumor cell drug resistance through the cGMP-PKG signaling pathway.</div></div><div><h3>Conclusion</h3><div>Our study demonstrates that APOA1-AS is a potential key regulator in colorectal cancer development and progression. It functions via glucose metabolism reprogramming and the cGMP-PKG signaling pathway, offering a novel therapeutic target for colorectal cancer.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"80 ","pages":"Article 102017"},"PeriodicalIF":2.3,"publicationDate":"2025-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143076122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Serum vault RNA1-1 levels reflect blood cells and bone marrow

IF 2.3 3区生物学 Q3 BIOCHEMICAL RESEARCH METHODS

Molecular and Cellular Probes

Pub Date : 2025-02-12 DOI: 10.1016/j.mcp.2025.102018

Yuki Hatayama , Hisashi Shimohiro , Yuki Hashimoto , Hitomi Ichikawa , Koji Kawamura , Toru Motokura

Introduction

Vault RNA1-1 (vtRNA1-1) exhibits antiviral and anti-apoptotic effects in infected and malignant cells. We observed that vtRNA1-1 levels in serum fluctuate in patients with hematological disorders, but its extracellular functions remain unclear. This study evaluates the potential of serum vtRNA1-1 levels as a biomarker for hematological disorders and investigates its association with bone marrow cell density (BMC).

Methods

Blood and serum samples were collected from patients with hematological disorders, patients who underwent bone marrow examination, PBSCT donors, and AML patients who received chemotherapy. VtRNA1-1 levels were measured using real-time quantitative RT-PCR. BMC was calculated by digital image analysis, and multiple regression analysis was performed using serum vtRNA1-1 and hematological and biochemical data as explanatory variables.

Results

The vtRNA1-1 levels in the blood of 11 patients with hematological disorders averaged 10.8 log₁₀ cps/ml, significantly higher than 8.4 log₁₀ cps/ml in serum. Multiple regression analysis estimated the vtRNA1-1 expression levels of each blood cell. In 87 patients who underwent bone marrow examination, there was a significant correlation between serum vtRNA1-1 levels and BMC (Rs = 0.24, P = 0.023). In PBSCT donors, serum vtRNA1-1 levels increased after G-CSF administration (P < 0.001), and in AML patients, serum vtRNA1-1 levels decreased after the initiation of chemotherapy, fluctuating in parallel with white blood cell counts.

Conclusions

Our findings suggest that serum vtRNA1-1, derived from peripheral blood and bone marrow cells, can potentially serve as a clinical biomarker in specific diseases.

{"title":"Serum vault RNA1-1 levels reflect blood cells and bone marrow","authors":"Yuki Hatayama , Hisashi Shimohiro , Yuki Hashimoto , Hitomi Ichikawa , Koji Kawamura , Toru Motokura","doi":"10.1016/j.mcp.2025.102018","DOIUrl":"10.1016/j.mcp.2025.102018","url":null,"abstract":"<div><h3>Introduction</h3><div>Vault RNA1-1 (vtRNA1-1) exhibits antiviral and anti-apoptotic effects in infected and malignant cells. We observed that vtRNA1-1 levels in serum fluctuate in patients with hematological disorders, but its extracellular functions remain unclear. This study evaluates the potential of serum vtRNA1-1 levels as a biomarker for hematological disorders and investigates its association with bone marrow cell density (BMC).</div></div><div><h3>Methods</h3><div>Blood and serum samples were collected from patients with hematological disorders, patients who underwent bone marrow examination, PBSCT donors, and AML patients who received chemotherapy. VtRNA1-1 levels were measured using real-time quantitative RT-PCR. BMC was calculated by digital image analysis, and multiple regression analysis was performed using serum vtRNA1-1 and hematological and biochemical data as explanatory variables.</div></div><div><h3>Results</h3><div>The vtRNA1-1 levels in the blood of 11 patients with hematological disorders averaged 10.8 log<sub>10</sub> cps/ml, significantly higher than 8.4 log<sub>10</sub> cps/ml in serum. Multiple regression analysis estimated the vtRNA1-1 expression levels of each blood cell. In 87 patients who underwent bone marrow examination, there was a significant correlation between serum vtRNA1-1 levels and BMC (Rs = 0.24, P = 0.023). In PBSCT donors, serum vtRNA1-1 levels increased after G-CSF administration (P < 0.001), and in AML patients, serum vtRNA1-1 levels decreased after the initiation of chemotherapy, fluctuating in parallel with white blood cell counts.</div></div><div><h3>Conclusions</h3><div>Our findings suggest that serum vtRNA1-1, derived from peripheral blood and bone marrow cells, can potentially serve as a clinical biomarker in specific diseases.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"80 ","pages":"Article 102018"},"PeriodicalIF":2.3,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143383913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Clinical significance analysis of microRNA-199a-3p in gingival crevicular fluid for patients with chronic periodontitis

IF 2.3 3区生物学 Q3 BIOCHEMICAL RESEARCH METHODS

Molecular and Cellular Probes

Pub Date : 2025-02-12 DOI: 10.1016/j.mcp.2025.102015

Kaixuan Yan, Yu Zheng, Jing Liu, Shuo Li, Wei Si

Objective

The aim was to investigate the clinical performance of microRNA-199a-3p (miR-199a-3p) in patients with chronic periodontitis.

Methods

91 patients with chronic periodontitis and 78 healthy individuals were enrolled for the research subjects. MiR-199a-3p expression was detected using real-time quantitative PCR (RT-qPCR) assay. Pearson correlation analysis was used for the relevance of miR-199a-3p with inflammatory mediators. Receiver operating characteristic (ROC) and logistic regression were conducted for the evaluation of the diagnostic performance and risk factors of chronic periodontitis. Bioinformatics analysis was utilized for miR-199a-3p-related genes.

Results

MiR-199a-3p was distinctly decreased in gingival crevicular fluid from patients with chronic periodontitis. The area under the curve (AUC) was 0.978 to discriminate chronic periodontitis patients from healthy individuals. The negative correlation was observed between miR-199a-3p and inflammatory factors. Logistic regression showed that miR-199a-3p was an independently protective factor for the occurrence of chronic periodontitis. Bioinformatics analysis revealed that the predictive regulated genes of miR-199a-3p mainly concentrated in inflammatory-associated signaling pathways.

Conclusion

MiR-199a-3p was attenuated in patients with chronic periodontitis and an underlying diagnostic biomarker for the disease.

{"title":"Clinical significance analysis of microRNA-199a-3p in gingival crevicular fluid for patients with chronic periodontitis","authors":"Kaixuan Yan, Yu Zheng, Jing Liu, Shuo Li, Wei Si","doi":"10.1016/j.mcp.2025.102015","DOIUrl":"10.1016/j.mcp.2025.102015","url":null,"abstract":"<div><h3>Objective</h3><div>The aim was to investigate the clinical performance of microRNA-199a-3p (miR-199a-3p) in patients with chronic periodontitis.</div></div><div><h3>Methods</h3><div>91 patients with chronic periodontitis and 78 healthy individuals were enrolled for the research subjects. MiR-199a-3p expression was detected using real-time quantitative PCR (RT-qPCR) assay. Pearson correlation analysis was used for the relevance of miR-199a-3p with inflammatory mediators. Receiver operating characteristic (ROC) and logistic regression were conducted for the evaluation of the diagnostic performance and risk factors of chronic periodontitis. Bioinformatics analysis was utilized for miR-199a-3p-related genes.</div></div><div><h3>Results</h3><div>MiR-199a-3p was distinctly decreased in gingival crevicular fluid from patients with chronic periodontitis. The area under the curve (AUC) was 0.978 to discriminate chronic periodontitis patients from healthy individuals. The negative correlation was observed between miR-199a-3p and inflammatory factors. Logistic regression showed that miR-199a-3p was an independently protective factor for the occurrence of chronic periodontitis. Bioinformatics analysis revealed that the predictive regulated genes of miR-199a-3p mainly concentrated in inflammatory-associated signaling pathways.</div></div><div><h3>Conclusion</h3><div>MiR-199a-3p was attenuated in patients with chronic periodontitis and an underlying diagnostic biomarker for the disease.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"80 ","pages":"Article 102015"},"PeriodicalIF":2.3,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

THBS1 knockdown suppresses pancreatic cancer progression through JAK2/STAT3 signaling pathway THBS1敲低通过JAK2/STAT3信号通路抑制胰腺癌进展

IF 2.3 3区生物学 Q3 BIOCHEMICAL RESEARCH METHODS

Molecular and Cellular Probes

Pub Date : 2025-02-01 DOI: 10.1016/j.mcp.2024.102003

Ping Li , Kaixuan Wang , Jian Song , Zhuang Chen , Yongyu Li , Zhaowei Chen

Background

Thrombospondin 1 (THBS1), a secreted protein, is implicated in the progression of numerous cancers, yet its specific contributions to pancreatic cancer (PC) remain underexplored.

Methods

The association between THBS1 levels and prognosis in PC was investigated. Functional experiments in vitro were used to determine the cell functions of siTHBS1 through CCK8 assay for cell proliferation, Muse® Cell Analyzer for apoptosis, and transwell assay for invasion and migration. Colivelin was applied in recovery experiment to investigate the mechanism of THBS1 regulating the JAK2/STAT3 pathway in BXPC-3 cell. In addition, the LV-shTHBS1 lentivirus was used to construct subcutaneous tumors in nude mice to verify the function of THBS1 in vivo.

Results

THBS1 expression was elevated in PC and associated with a poorer prognosis. THBS1 was highly expressed in these PC cells. siTHBS1 repressed cell growth, migration and invasiveness, while promoting apoptosis of BXPC-3 cells. THBS1 suppression also led to a decrease in the phosphorylation of JAK2 and STAT3. JAK2/STAT3 signaling activator (Colivelin) could partially reverse the biological effects. In addition, shTHBS1 can suppress the growth of implanted tumors in nude mice.

Conclusions

THBS1 knockdown suppressed cell proliferation, migration, and invasion while enhanced cell apoptosis through the JAK2/STAT3 signaling pathway.

背景：血栓反应蛋白1 （THBS1）是一种分泌蛋白，与许多癌症的进展有关，但其对胰腺癌（PC）的特异性贡献仍未得到充分研究。方法：探讨原发性肝癌患者THBS1水平与预后的关系。体外功能实验通过CCK8法检测细胞增殖，Muse®细胞分析仪检测细胞凋亡，transwell法检测细胞侵袭和迁移，检测siTHBS1的细胞功能。利用Colivelin进行恢复实验，探讨THBS1调控BXPC-3细胞JAK2/STAT3通路的机制。此外，我们利用LV-shTHBS1慢病毒在裸鼠体内构建皮下肿瘤，验证THBS1在体内的功能。结果：THBS1在PC中表达升高，预后较差。THBS1在这些PC细胞中高表达。siTHBS1抑制BXPC-3细胞的生长、迁移和侵袭，同时促进BXPC-3细胞的凋亡。THBS1抑制也导致JAK2和STAT3磷酸化水平降低。JAK2/STAT3信号激活因子Colivelin可以部分逆转生物学效应。此外，shTHBS1还能抑制裸鼠植入式肿瘤的生长。结论：THBS1敲低可通过JAK2/STAT3信号通路抑制细胞增殖、迁移和侵袭，同时增强细胞凋亡。

{"title":"THBS1 knockdown suppresses pancreatic cancer progression through JAK2/STAT3 signaling pathway","authors":"Ping Li , Kaixuan Wang , Jian Song , Zhuang Chen , Yongyu Li , Zhaowei Chen","doi":"10.1016/j.mcp.2024.102003","DOIUrl":"10.1016/j.mcp.2024.102003","url":null,"abstract":"<div><h3>Background</h3><div>Thrombospondin 1 (THBS1), a secreted protein, is implicated in the progression of numerous cancers, yet its specific contributions to pancreatic cancer (PC) remain underexplored.</div></div><div><h3>Methods</h3><div>The association between THBS1 levels and prognosis in PC was investigated. Functional experiments <em>in vitro</em> were used to determine the cell functions of siTHBS1 through CCK8 assay for cell proliferation, Muse® Cell Analyzer for apoptosis, and transwell assay for invasion and migration. Colivelin was applied in recovery experiment to investigate the mechanism of THBS1 regulating the JAK2/STAT3 pathway in BXPC-3 cell. In addition, the LV-shTHBS1 lentivirus was used to construct subcutaneous tumors in nude mice to verify the function of THBS1 <em>in vivo</em>.</div></div><div><h3>Results</h3><div>THBS1 expression was elevated in PC and associated with a poorer prognosis. THBS1 was highly expressed in these PC cells. siTHBS1 repressed cell growth, migration and invasiveness, while promoting apoptosis of BXPC-3 cells. THBS1 suppression also led to a decrease in the phosphorylation of JAK2 and STAT3. JAK2/STAT3 signaling activator (Colivelin) could partially reverse the biological effects. In addition, shTHBS1 can suppress the growth of implanted tumors in nude mice.</div></div><div><h3>Conclusions</h3><div>THBS1 knockdown suppressed cell proliferation, migration, and invasion while enhanced cell apoptosis through the JAK2/STAT3 signaling pathway.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"79 ","pages":"Article 102003"},"PeriodicalIF":2.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142878328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LncRNA TMC3-AS1 silence alleviates lipopolysaccharide-induced acute kidney injury by suppressing Wnt5a-mediated autophagy and pyroptosis pathway LncRNA TMC3-AS1沉默通过抑制wnt5a介导的自噬和焦亡途径减轻脂多糖诱导的急性肾损伤。

IF 2.3 3区生物学 Q3 BIOCHEMICAL RESEARCH METHODS

Molecular and Cellular Probes

Pub Date : 2025-02-01 DOI: 10.1016/j.mcp.2024.102006

Jing Guo , Rao Fu , Bo Zhao , Hongbo Li , Jundong Jiao

Long non-coding RNA TMC3-AS1 is identified to be upregulated by lipopolysaccharide (LPS) in inflammatory disease, but its role in acute kidney injury (AKI) is almost unknown. The study investigated the involvement of TMC3-AS1 in LPS-induced AKI and its downstream molecular regulatory mechanism. Our data suggested that knocking down TMC3-AS1 significantly reduced renal dysfunction, tissue inflammation and tissue damage in LPS-induced mice, and promoted cell viability, inhibited inflammation, apoptosis and necrosis in LPS-stimulated human renal tubular epithelial cells HK2. Meanwhile, silencing TMC3-AS1 decreased the expression levels of Wnt5a, Atg5, NLRP3 and cleaved caspase1 and the ratio of LC3II/LC3I, but elevated p62 level in vivo and in vitro, suggesting the inhibitory effect of TMC3-AS1 silence on Wnt5a signaling, autophagy, and pyroptosis. Mechanically, TMC3-AS1 upregulated the expression of WNT5A mRNA and Wnt5a protein through competitively binding with miR-148a-3p, thus elevating the expression levels of autophagy and pyroptosis-associated markers in LPS-induced HK2 cells. MiR-148a-3p mimic also exerted protective effects on LPS-treated HK2 cells, which was counteracted by overexpressing WNT5A or TMC3-AS1. Altogether, these findings reveal that TMC3-AS1 inhibition restrains LPS-triggered AKI progression through inactivating Wnt5a -mediated autophagy and pyroptosis pathway.

长链非编码RNA TMC3-AS1在炎症性疾病中被脂多糖（LPS）上调，但其在急性肾损伤（AKI）中的作用几乎未知。本研究探讨了TMC3-AS1参与lps诱导的AKI及其下游分子调控机制。我们的数据表明，敲低TMC3-AS1可显著减轻lps诱导小鼠的肾功能障碍、组织炎症和组织损伤，提高lps刺激的人肾小管上皮细胞HK2的细胞活力，抑制炎症、凋亡和坏死。同时，沉默TMC3-AS1可降低Wnt5a、Atg5、NLRP3和cleaved caspase1的表达水平及LC3II/LC3I比值，但提高体内外p62水平，提示沉默TMC3-AS1对Wnt5a信号通路、自噬和焦亡有抑制作用。机械上，TMC3-AS1通过与miR-148a-3p的竞争性结合上调WNT5A mRNA和WNT5A蛋白的表达，从而提高lps诱导的HK2细胞中自噬和热噬相关标志物的表达水平。MiR-148a-3p mimic对lps处理的HK2细胞也有保护作用，但这种作用会被过表达WNT5A或TMC3-AS1所抵消。总之，这些发现表明TMC3-AS1抑制通过灭活Wnt5a介导的自噬和焦亡途径抑制lps触发的AKI进展。

{"title":"LncRNA TMC3-AS1 silence alleviates lipopolysaccharide-induced acute kidney injury by suppressing Wnt5a-mediated autophagy and pyroptosis pathway","authors":"Jing Guo , Rao Fu , Bo Zhao , Hongbo Li , Jundong Jiao","doi":"10.1016/j.mcp.2024.102006","DOIUrl":"10.1016/j.mcp.2024.102006","url":null,"abstract":"<div><div>Long non-coding RNA TMC3-AS1 is identified to be upregulated by lipopolysaccharide (LPS) in inflammatory disease, but its role in acute kidney injury (AKI) is almost unknown. The study investigated the involvement of TMC3-AS1 in LPS-induced AKI and its downstream molecular regulatory mechanism. Our data suggested that knocking down TMC3-AS1 significantly reduced renal dysfunction, tissue inflammation and tissue damage in LPS-induced mice, and promoted cell viability, inhibited inflammation, apoptosis and necrosis in LPS-stimulated human renal tubular epithelial cells HK2. Meanwhile, silencing TMC3-AS1 decreased the expression levels of Wnt5a, Atg5, NLRP3 and cleaved caspase1 and the ratio of LC3II/LC3I, but elevated p62 level <em>in vivo</em> and <em>in vitro</em>, suggesting the inhibitory effect of TMC3-AS1 silence on Wnt5a signaling, autophagy, and pyroptosis. Mechanically, TMC3-AS1 upregulated the expression of WNT5A mRNA and Wnt5a protein through competitively binding with miR-148a-3p, thus elevating the expression levels of autophagy and pyroptosis-associated markers in LPS-induced HK2 cells. MiR-148a-3p mimic also exerted protective effects on LPS-treated HK2 cells, which was counteracted by overexpressing WNT5A or TMC3-AS1. Altogether, these findings reveal that TMC3-AS1 inhibition restrains LPS-triggered AKI progression through inactivating Wnt5a -mediated autophagy and pyroptosis pathway.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"79 ","pages":"Article 102006"},"PeriodicalIF":2.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142899969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Uncovering molecular sensitization patterns for peanut in East-Central European children: The dominance of Ara h 6 揭示花生在中东欧儿童中的分子致敏模式：Ara h6的优势。

IF 2.3 3区生物学 Q3 BIOCHEMICAL RESEARCH METHODS

Molecular and Cellular Probes

Pub Date : 2025-02-01 DOI: 10.1016/j.mcp.2025.102009

Gabriella Páll , Tamás Pándics , Erzsébet Pintér , Mária Kun , Anna Karoliny , Lajos A. Réthy

引用次数: 0

The application of CRISPR/Cas9–based genome-wide screening to disease research 基于CRISPR/ cas9的全基因组筛选在疾病研究中的应用

IF 2.3 3区生物学 Q3 BIOCHEMICAL RESEARCH METHODS

Molecular and Cellular Probes

Pub Date : 2025-02-01 DOI: 10.1016/j.mcp.2024.102004

Xiuqin Chen , Min Zheng , Su Lin , Meiqing Huang , Shaoying Chen , Shilong Chen

High-throughput genetic screening serves as an indispensable approach for deciphering gene functions and the intricate relationships between phenotypes and genotypes. The CRISPR/Cas9 system, with its ability to precisely edit genomes on a large scale, has revolutionized the field by enabling the construction of comprehensive genomic libraries. This technology has become a cornerstone for genome-wide screenings in disease research. This review offers a comprehensive examination of how CRISPR/Cas9-based genetic screening has been leveraged to uncover genes that play a role in disease mechanisms, focusing on areas such as cancer development and viral replication processes. The insights presented in this review hold promise for the development of novel therapeutic strategies and precision medicine approaches.

高通量遗传筛选是解读基因功能和表型与基因型之间复杂关系的重要手段。CRISPR/Cas9系统具有大规模精确编辑基因组的能力，通过构建全面的基因组文库，使该领域发生了革命性的变化。这项技术已经成为疾病研究中全基因组筛选的基石。这篇综述全面研究了基于CRISPR/ cas9的基因筛选如何被利用来发现在疾病机制中发挥作用的基因，重点关注癌症发展和病毒复制过程等领域。本综述提出的见解为开发新的治疗策略和精确医学方法提供了希望。

引用次数: 0

Comprehensive analysis of Apigetrin's effects on liver cancer cells: Insights from bioinformatics, in vitro studies, and next-generation transcriptome sequencing

IF 2.3 3区生物学 Q3 BIOCHEMICAL RESEARCH METHODS

Molecular and Cellular Probes

Pub Date : 2025-02-01 DOI: 10.1016/j.mcp.2025.102012

Pritam Bhagwan Bhosale , Abuyaseer Abusaliya , Hun Hwan Kim , Vetrivel Preethi , Se Hyo Jeong , Min Yeong Park , Chung Kil Won , Jeong Doo Heo , Meejung Ahn , Je Kyung Seong , Gon Sup Kim

Despite numerous attempts to understand the molecular mechanisms behind the development of liver cancer, it continues to pose a significant worldwide health challenge. Transcriptome sequencing, a powerful tool in molecular biology, has played a pivotal role in uncovering the intricate gene expression profiles underlying hepatocellular carcinoma (HCC). In the present study, we identified a total of 808 differentially expressed genes (DEGs), with 584 exhibiting downregulation, and 224 showing upregulation following apigetrin treatment. We utilized a combination of bioinformatics tools and platforms, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment and mapping, Protein-Protein Interaction (PPI), and GEPIA. We found that DEGs were related to the apoptotic cell death process and identified hub genes, namely CASP8, RB1, and TGFBR2. These genes were further validated through both GEPIA analysis and western blot experiments. Our findings collectively demonstrate that apigetrin has the potential to modulate genes related to liver cancer and trigger molecular pathways that lead to apoptotic cell death in liver cancer cells. This study underscores the potential of apigetrin as an innovative treatment strategy for HCC, emphasizing the need for additional research to elucidate its mechanisms of action and evaluate its clinical efficacy.

{"title":"Comprehensive analysis of Apigetrin's effects on liver cancer cells: Insights from bioinformatics, in vitro studies, and next-generation transcriptome sequencing","authors":"Pritam Bhagwan Bhosale , Abuyaseer Abusaliya , Hun Hwan Kim , Vetrivel Preethi , Se Hyo Jeong , Min Yeong Park , Chung Kil Won , Jeong Doo Heo , Meejung Ahn , Je Kyung Seong , Gon Sup Kim","doi":"10.1016/j.mcp.2025.102012","DOIUrl":"10.1016/j.mcp.2025.102012","url":null,"abstract":"<div><div>Despite numerous attempts to understand the molecular mechanisms behind the development of liver cancer, it continues to pose a significant worldwide health challenge. Transcriptome sequencing, a powerful tool in molecular biology, has played a pivotal role in uncovering the intricate gene expression profiles underlying hepatocellular carcinoma (HCC). In the present study, we identified a total of 808 differentially expressed genes (DEGs), with 584 exhibiting downregulation, and 224 showing upregulation following apigetrin treatment. We utilized a combination of bioinformatics tools and platforms, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment and mapping, Protein-Protein Interaction (PPI), and GEPIA. We found that DEGs were related to the apoptotic cell death process and identified hub genes, namely CASP8, RB1, and TGFBR2. These genes were further validated through both GEPIA analysis and western blot experiments. Our findings collectively demonstrate that apigetrin has the potential to modulate genes related to liver cancer and trigger molecular pathways that lead to apoptotic cell death in liver cancer cells. This study underscores the potential of apigetrin as an innovative treatment strategy for HCC, emphasizing the need for additional research to elucidate its mechanisms of action and evaluate its clinical efficacy.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"79 ","pages":"Article 102012"},"PeriodicalIF":2.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143048647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0