Pub Date : 2023-01-01DOI: 10.32604/biocell.2023.026911
Lakshana Sadu, R. Krishnan, R. L. Akshaya, I. Saranya, Udipt RANJAN DAS, Sneha Satishkumar, N. Selvamurugan
{"title":"Roles of miR-214 in bone physiology and disease","authors":"Lakshana Sadu, R. Krishnan, R. L. Akshaya, I. Saranya, Udipt RANJAN DAS, Sneha Satishkumar, N. Selvamurugan","doi":"10.32604/biocell.2023.026911","DOIUrl":"https://doi.org/10.32604/biocell.2023.026911","url":null,"abstract":"","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"21 1","pages":""},"PeriodicalIF":1.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91104154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.32604/biocell.2023.027971
Miaomiao Li, Z. Zheng, Junyi Ke, Jieyi Luo, Fan Jiang, Yan-xia Qu, B. Zhu, Yinghua Li, Liandong Zuo
{"title":"Inhibition of H2O2-induced TM3 cell apoptosis by oxidative stress by lentinan functionalized selenium nanoparticles through JAK2/STAT-3 and P53 pathways","authors":"Miaomiao Li, Z. Zheng, Junyi Ke, Jieyi Luo, Fan Jiang, Yan-xia Qu, B. Zhu, Yinghua Li, Liandong Zuo","doi":"10.32604/biocell.2023.027971","DOIUrl":"https://doi.org/10.32604/biocell.2023.027971","url":null,"abstract":"","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"30 1","pages":""},"PeriodicalIF":1.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83351544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.32604/biocell.2023.027677
SHENGJIE SONG, ZHIZHOU SHI
Metabolic reprogramming frequently occurs in the majority of cancers, wherein fatty acid oxidation (FAO) is usually induced and serves as a compensatory mechanism to improve energy consumption. Carnitine palmitoyltransferase 1A (CPT1A) is the rate-limiting enzyme for FAO and is widely involved in tumor growth, metastasis, and chemo-/radio-resistance. This review summarizes the most recent advances in understanding the oncogenic roles and mechanisms of CPT1A in tumorigenesis, including in proliferation and tumor growth, invasion and metastasis, and the tumor microenvironment. Importantly, CPT1A has been shown to be a biomarker for diagnosis and prognosis prediction and proved to be a candidate therapeutic target, especially for the treatment of drug- and radiation-resistant tumors. In summary, CPT1A plays remarkable roles in promoting cancer progression and is a potential anticancer therapeutic target.
{"title":"CPT1A in cancer: Tumorigenic roles and therapeutic implications","authors":"SHENGJIE SONG, ZHIZHOU SHI","doi":"10.32604/biocell.2023.027677","DOIUrl":"https://doi.org/10.32604/biocell.2023.027677","url":null,"abstract":"Metabolic reprogramming frequently occurs in the majority of cancers, wherein fatty acid oxidation (FAO) is usually induced and serves as a compensatory mechanism to improve energy consumption. Carnitine palmitoyltransferase 1A (CPT1A) is the rate-limiting enzyme for FAO and is widely involved in tumor growth, metastasis, and chemo-/radio-resistance. This review summarizes the most recent advances in understanding the oncogenic roles and mechanisms of CPT1A in tumorigenesis, including in proliferation and tumor growth, invasion and metastasis, and the tumor microenvironment. Importantly, CPT1A has been shown to be a biomarker for diagnosis and prognosis prediction and proved to be a candidate therapeutic target, especially for the treatment of drug- and radiation-resistant tumors. In summary, CPT1A plays remarkable roles in promoting cancer progression and is a potential anticancer therapeutic target.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"267 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135505521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.32604/biocell.2023.030383
PAVITHRA SUBRAMANI, RAUNAK KUMAR DAS
Solar ultraviolet B (UVB) radiation is a major skin cancer-causing agent. Initiation, promotion, and progression are the diverse phases of UVB-induced carcinogenesis. Exposure to UVB causes abnormalities in a series of biochemical and molecular pathways: thymine dimer formation, DNA damage, oxidative stress, inflammatory responses, and altered cell signaling, eventually resulting in tumor formation. The increased skin cancer rates urge researchers to develop more efficient drugs, but synthetic chemotherapeutic drugs have more contrary effects and drug resistance issues, which have been reported recently. The current review focuses on the relationship between microbes and cancer. Human skin acts as a barrier against the external environment and serves as a protective shield for its inhabitant microbiota, collectively called skin microbes. The gut microbiome plays a vital role in cancer therapy. Production of short-chain fatty acids (SCFAs) such as butyrate, acetate, and propionate by intestinal microbes has anti-cancer properties against various cancer cell lines. Yet, the knowledge of SCFAs produced by skin microbes remains yet to be elucidated exhaustively. In this review, we strive to summarize the findings of studies performed to date regarding the anti-cancer properties of SCFA against various cancer cell lines and provide insight into future directions in the skin microbiome field.
{"title":"Possible therapeutic role of short-chain fatty acids from skin commensal bacteria in UVB-induced skin carcinogenesis","authors":"PAVITHRA SUBRAMANI, RAUNAK KUMAR DAS","doi":"10.32604/biocell.2023.030383","DOIUrl":"https://doi.org/10.32604/biocell.2023.030383","url":null,"abstract":"Solar ultraviolet B (UVB) radiation is a major skin cancer-causing agent. Initiation, promotion, and progression are the diverse phases of UVB-induced carcinogenesis. Exposure to UVB causes abnormalities in a series of biochemical and molecular pathways: thymine dimer formation, DNA damage, oxidative stress, inflammatory responses, and altered cell signaling, eventually resulting in tumor formation. The increased skin cancer rates urge researchers to develop more efficient drugs, but synthetic chemotherapeutic drugs have more contrary effects and drug resistance issues, which have been reported recently. The current review focuses on the relationship between microbes and cancer. Human skin acts as a barrier against the external environment and serves as a protective shield for its inhabitant microbiota, collectively called skin microbes. The gut microbiome plays a vital role in cancer therapy. Production of short-chain fatty acids (SCFAs) such as butyrate, acetate, and propionate by intestinal microbes has anti-cancer properties against various cancer cell lines. Yet, the knowledge of SCFAs produced by skin microbes remains yet to be elucidated exhaustively. In this review, we strive to summarize the findings of studies performed to date regarding the anti-cancer properties of SCFA against various cancer cell lines and provide insight into future directions in the skin microbiome field.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"14 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135504584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.32604/biocell.2023.030147
LIANLI NI, YUN YU, HAN LIN, WEISHAN ZHUGE, LU TAO, YIWEI SHEN, RI CUI, SHAOTANG LI
Background: Homeobox B8 (HOXB8), a member of HOX family, plays a key role in the development of colorectal cancer (CRC). However, the function of HOXB8 in oxaliplatin (OXA) resistance in CRC is still unclear. This study investigated the role and precise molecular mechanism of HOXB8 in OXA-resistant CRC cells. Methods: The cell viability was measured by the 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay, and the colony forming ability was determined by colony formation assay. The silencing RNA (siRNA) approach was used to knockdown HOXB8 in CRC cells while the lentiviral transfection system was used to establish stable HOXB8 overexpressing CRC cells. The protein and mRNA levels were evaluated by western blot and real-time reverse transcription-polymerase chain reaction. Results: HOXB8 expression was upregulated in OXA-resistant HCT116 cells (HCT116/OXA) compared to its level in the parent HCT116 cells. Knockdown of HOXB8 significantly inhibited CRC cell growth by suppressing the signal transducer and activator of transcription 3 (STAT3) pathway. HOXB8 knockdown also potentiated cytotoxicity of OXA in CRC cells. Inversely, HOXB8 overexpression attenuated OXA-induced growth inhibition of HCT116 cells and RKO cells by activating STAT3 signaling. HOXB8 knockdown effectively inhibited HCT116/OXA cell viability regardless of OXA treatment by suppressing STAT3 signaling. Conclusions: These results shed light on the important functions of HOXB8 in OXA-resistant CRC and suggested that targeting HOXB8 might be an effective therapeutic strategy for select OXA-resistant CRC patients.
背景:Homeobox B8 (HOXB8)是HOX家族成员之一，在结直肠癌(CRC)的发生发展中起着关键作用。然而，HOXB8在大肠癌奥沙利铂(OXA)耐药中的作用尚不清楚。本研究探讨了HOXB8在oxa耐药CRC细胞中的作用及其精确的分子机制。方法:采用3-[4,5-二甲基噻唑-2-基]-2,5二苯基溴化四唑(MTT)法测定细胞活力，采用集落形成法测定细胞集落形成能力。采用沉默RNA (siRNA)方法敲低CRC细胞中的HOXB8，采用慢病毒转染系统建立稳定的过表达HOXB8的CRC细胞。western blot和实时逆转录-聚合酶链反应检测蛋白和mRNA水平。结果:与亲本HCT116细胞相比，HOXB8在OXA抗性HCT116细胞(HCT116/OXA)中的表达上调。敲低HOXB8可通过抑制STAT3 (signal transducer and activator of transcription 3)通路显著抑制CRC细胞生长。HOXB8敲低也增强了OXA在结直肠癌细胞中的细胞毒性。相反，HOXB8过表达通过激活STAT3信号通路减弱oxa诱导的HCT116细胞和RKO细胞的生长抑制。HOXB8敲低通过抑制STAT3信号传导有效抑制HCT116/OXA细胞活力，无论OXA是否治疗。结论:这些结果揭示了HOXB8在oxa耐药结直肠癌中的重要功能，并提示靶向HOXB8可能是治疗部分oxa耐药结直肠癌患者的有效策略。
{"title":"HOXB8 contributed to oxaliplatin chemo-resistance in colon cancer cells by activating STAT3","authors":"LIANLI NI, YUN YU, HAN LIN, WEISHAN ZHUGE, LU TAO, YIWEI SHEN, RI CUI, SHAOTANG LI","doi":"10.32604/biocell.2023.030147","DOIUrl":"https://doi.org/10.32604/biocell.2023.030147","url":null,"abstract":"<b>Background:</b> Homeobox B8 (HOXB8), a member of HOX family, plays a key role in the development of colorectal cancer (CRC). However, the function of HOXB8 in oxaliplatin (OXA) resistance in CRC is still unclear. This study investigated the role and precise molecular mechanism of HOXB8 in OXA-resistant CRC cells. <b>Methods:</b> The cell viability was measured by the 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay, and the colony forming ability was determined by colony formation assay. The silencing RNA (siRNA) approach was used to knockdown HOXB8 in CRC cells while the lentiviral transfection system was used to establish stable HOXB8 overexpressing CRC cells. The protein and mRNA levels were evaluated by western blot and real-time reverse transcription-polymerase chain reaction. <b>Results:</b> HOXB8 expression was upregulated in OXA-resistant HCT116 cells (HCT116/OXA) compared to its level in the parent HCT116 cells. Knockdown of HOXB8 significantly inhibited CRC cell growth by suppressing the signal transducer and activator of transcription 3 (STAT3) pathway. HOXB8 knockdown also potentiated cytotoxicity of OXA in CRC cells. Inversely, HOXB8 overexpression attenuated OXA-induced growth inhibition of HCT116 cells and RKO cells by activating STAT3 signaling. HOXB8 knockdown effectively inhibited HCT116/OXA cell viability regardless of OXA treatment by suppressing STAT3 signaling. <b>Conclusions:</b> These results shed light on the important functions of HOXB8 in OXA-resistant CRC and suggested that targeting HOXB8 might be an effective therapeutic strategy for select OXA-resistant CRC patients.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"56 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135505229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.32604/biocell.2023.029860
JIAZHUANG LI, WEI ZHANG, SHOUBAO GAO, LI SUN, QINGYANG TAI, YING LIU
{"title":"Long non-coding RNA-ATB induces trastuzumab resistance and aggravates the progression of gastric cancer by repressing miR- 200c via ZNF217 elevation","authors":"JIAZHUANG LI, WEI ZHANG, SHOUBAO GAO, LI SUN, QINGYANG TAI, YING LIU","doi":"10.32604/biocell.2023.029860","DOIUrl":"https://doi.org/10.32604/biocell.2023.029860","url":null,"abstract":"","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"8 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135556221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
: Objective: This study aimed to investigate the potential of human umbilical cord mesenchymal stem cell (hucMSC)-derived exosomes (hucMSC-Exos) in inhibiting hypoxia-induced cell hyper proliferation and overexpression of vascular endothelial growth factor A (VEGF-A) in immature human fetal retinal microvascular endothelial cells (hfRMECs). Methods: Exosomes were isolated from hucMSCs using cryogenic ultracentrifugation and characterized through various techniques, including transmission electron microscopy, nanoparticle tracking analysis, bicinchoninic acid assays, and western blotting. The hfRMECs were identi fi ed using von Willebrand factor (vWF) co-staining and divided into four groups: a control group cultured under normoxic condition, a hypoxic model group, a hypoxic group treated with low-concentration hucMSC-Exos (75 μ g/mL) and a hypoxic group treated with high-concentration hucMSC-Exos (100 μ g/mL). Cell viability and proliferation were assessed using Cell Counting Kit-8 (CCK-8) assay and EdU (5-ethynyl-2 ′ -deoxyuridine) assay respectively. Expression levels of VEGF-A were evaluated using RT-PCR, western blotting and immuno fl uorescence. Results: Hypoxia signi fi cantly increased hfRMECs ’ viability and proliferation by upregulating VEGF-A levels. The administration of hucMSC-Exos effectively reversed this response, with the high-concentration group exhibiting greater ef fi cacy compared to the low-concentration group. Conclusion: In conclusion, hucMSC-Exos can dose-dependently inhibit hypoxia-induced hyperproliferation and VEGF-A overexpression in immature fetal retinal microvascular endothelial cells.
{"title":"Inhibition of VEGF-A expression in hypoxia-exposed fetal retinal microvascular endothelial cells by exosomes derived from human umbilical cord mesenchymal stem cells","authors":"JING LI, WANWAN FAN, LILI HAO, YONGSHENG LI, GUOCHENG YU, WEI SUN, XIANQIONG LUO, JINGXIANG ZHONG","doi":"10.32604/biocell.2023.044177","DOIUrl":"https://doi.org/10.32604/biocell.2023.044177","url":null,"abstract":": Objective: This study aimed to investigate the potential of human umbilical cord mesenchymal stem cell (hucMSC)-derived exosomes (hucMSC-Exos) in inhibiting hypoxia-induced cell hyper proliferation and overexpression of vascular endothelial growth factor A (VEGF-A) in immature human fetal retinal microvascular endothelial cells (hfRMECs). Methods: Exosomes were isolated from hucMSCs using cryogenic ultracentrifugation and characterized through various techniques, including transmission electron microscopy, nanoparticle tracking analysis, bicinchoninic acid assays, and western blotting. The hfRMECs were identi fi ed using von Willebrand factor (vWF) co-staining and divided into four groups: a control group cultured under normoxic condition, a hypoxic model group, a hypoxic group treated with low-concentration hucMSC-Exos (75 μ g/mL) and a hypoxic group treated with high-concentration hucMSC-Exos (100 μ g/mL). Cell viability and proliferation were assessed using Cell Counting Kit-8 (CCK-8) assay and EdU (5-ethynyl-2 ′ -deoxyuridine) assay respectively. Expression levels of VEGF-A were evaluated using RT-PCR, western blotting and immuno fl uorescence. Results: Hypoxia signi fi cantly increased hfRMECs ’ viability and proliferation by upregulating VEGF-A levels. The administration of hucMSC-Exos effectively reversed this response, with the high-concentration group exhibiting greater ef fi cacy compared to the low-concentration group. Conclusion: In conclusion, hucMSC-Exos can dose-dependently inhibit hypoxia-induced hyperproliferation and VEGF-A overexpression in immature fetal retinal microvascular endothelial cells.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"18 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135563776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.32604/biocell.2023.026615
P. Solanki, Nisarg Rana, Prakash C. JHA, A. Manhas
{"title":"A comprehensive analysis of the role of molecular docking in the development of anticancer agents against the cell cycle CDK enzyme","authors":"P. Solanki, Nisarg Rana, Prakash C. JHA, A. Manhas","doi":"10.32604/biocell.2023.026615","DOIUrl":"https://doi.org/10.32604/biocell.2023.026615","url":null,"abstract":"","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"127 1","pages":""},"PeriodicalIF":1.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80392701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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