Cell Cycle最新文献_第4页

Evaluation of differences in expression pattern of three isoforms of the transforming growth factor beta in patients with lumbosacral stenosis. 评估腰骶椎管狭窄症患者体内转化生长因子 beta 三种同工酶表达模式的差异。

IF 4.3 3区生物学

Cell Cycle Pub Date : 2024-03-01 Epub Date: 2024-05-02 DOI: 10.1080/15384101.2024.2345484

Dawid Sobański, Paweł Bogdał, Rafał Staszkiewicz, Małgorzata Sobańska, Michał Filipowicz, Ryszard Adam Czepko, Damian Strojny, Beniamin Oskar Grabarek

{"title":"Evaluation of differences in expression pattern of three isoforms of the transforming growth factor beta in patients with lumbosacral stenosis.","authors":"Dawid Sobański, Paweł Bogdał, Rafał Staszkiewicz, Małgorzata Sobańska, Michał Filipowicz, Ryszard Adam Czepko, Damian Strojny, Beniamin Oskar Grabarek","doi":"10.1080/15384101.2024.2345484","DOIUrl":"10.1080/15384101.2024.2345484","url":null,"abstract":"The study investigates molecular changes in the lumbosacral (L/S) spine's yellow ligamentum flavum during degenerative stenosis, focusing on the role of transforming growth factor beta 1-3 (TGF-β-1-3). Sixty patients with degenerative stenosis and sixty control participants underwent molecular analysis using real-time quantitative reverse transcription reaction technique (RTqPCR), enzyme-linked immunosorbent assay (ELISA), Western blot, and immunohistochemical analysis (IHC). At the mRNA level, study samples showed reduced expression of TGF-β-1 and TGF-β-3, while TGF-β-2 increased by only 4%. Conversely, at the protein level, the study group exhibited significantly higher concentrations of TGF-β-1, TGF-β-2, and TGF-β-3 compared to controls. On the other hand, at the protein level, a statistically significant higher concentration of TGF-β-1 was observed (2139.33 pg/mL ± 2593.72 pg/mL vs. 252.45 pg/mL ± 83.89 pg/mL; p < 0.0001), TGF-β-2 (3104.34 pg/mL ± 1192.74 pg/mL vs. 258.86 pg/mL ± 82.98 pg/mL; p < 0.0001), TGF-β-3 (512.75 pg/mL ± 107.36 pg/mL vs. 55.06 pg/mL ± 9.83 pg/mL, p < 0.0001) in yellow ligaments obtained from patients of the study group compared to control samples. The study did not establish a significant correlation between TGF-β-1-3 concentrations and pain severity. The findings suggest that molecular therapy aimed at restoring the normal expression pattern of TGF-β-1-3 could be a promising strategy for treating degenerative stenosis of the L/S spine. The study underscores the potential therapeutic significance of addressing molecular changes at the TGF-β isoforms level for better understanding and managing degenerative spinal conditions.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11135850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140847891","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

Pumilio RNA binding family member 1 deficiency activates anti-tumor immunity in hepatocellular carcinoma via restraining M2 macrophage polarization. Pumilio RNA 结合家族成员 1 缺乏症可通过抑制 M2 巨噬细胞极化激活肝细胞癌的抗肿瘤免疫。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2024-03-01 Epub Date: 2024-05-24 DOI: 10.1080/15384101.2024.2355825

Yang Yu, Gang Nie, Yi-Wei Ren, Liu Ouyang, Chen-Ming Ni

引用次数: 0

Knock down of APE1 suppressed gastric cancer metastasis via improving immune disorders caused by myeloid-derived suppressor cells. 通过改善髓源性抑制细胞导致的免疫紊乱，敲除 APE1 可抑制胃癌转移。

IF 4.3 3区生物学

Cell Cycle Pub Date : 2024-03-01 Epub Date: 2024-05-08 DOI: 10.1080/15384101.2024.2351629

Baoming Zhang, Qiang Tang, Wenchao Shi, Zengtao Bao, Shanting Gao, Cheng Pan

{"title":"Knock down of APE1 suppressed gastric cancer metastasis via improving immune disorders caused by myeloid-derived suppressor cells.","authors":"Baoming Zhang, Qiang Tang, Wenchao Shi, Zengtao Bao, Shanting Gao, Cheng Pan","doi":"10.1080/15384101.2024.2351629","DOIUrl":"10.1080/15384101.2024.2351629","url":null,"abstract":"Gastric cancer is a highly immunogenic malignancy. Immune tolerance facilitated by myeloid-derived suppressor cells (MDSCs) has been implicated in gastric cancer resistance mechanisms. The potential role of APE1 in regulating gastric cancer metastasis by targeting MDSCs remains uncertain. In this study, the plasmid Plxpsp-mGM-CSF was used to induce high expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) in GES-1 cells. For tumor transplantation experiments, AGS, AGS+GM-CSF and AGS+GM-CSF-siAPE1 cell lines were established by transfection, followed by subcutaneous implantation of tumor cells. MDSCs, Treg cells, IgG, CD3 and CD8 levels were assessed. Transfection with siAPE1 significantly inhibited tumor growth compared to the AGS+GM-CSF group. APE1 gene knockdown modulated the immune system in gastric cancer mice, characterized by a decrease in MDSCs and an increase in Treg cells, IgG, CD3 and CD8. In addition, APE1 gene knockdown resulted in decreased levels of pro-MDSC cytokines (HGF, CCL5, IL-6, CCL12). Furthermore, APE1 gene knockdown inhibited proliferation, migration and invasion of AGS and MKN45 cells. AGS-GM-CSF cell transplantation increased MDSC levels and accelerated tumor growth, whereas APE1 knockdown reduced MDSC levels, inhibited tumor growth and attenuated inflammatory infiltration in gastric cancer tissues. Strategies targeting the APE1/MDSC axis offer a promising approach to the prevention and treatment of gastric cancer, providing new insights into its management.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11135849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140891474","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

Hsa_circ_0079875 functions as a competitive endogenous RNA to promote hepatocellular carcinoma progression. Hsa_circ_0079875 作为一种竞争性内源性 RNA，具有促进肝细胞癌进展的功能。

IF 4.3 3区生物学

Cell Cycle Pub Date : 2024-03-01 Epub Date: 2024-04-29 DOI: 10.1080/15384101.2024.2345469

Yicun Liu, Xi Luo, WeiJie Chen, Zhixing Dong, Tiaochun Cheng, Lin Chen, Linling Ju, Weihua Cai, Zhaolian Bian

{"title":"Hsa_circ_0079875 functions as a competitive endogenous RNA to promote hepatocellular carcinoma progression.","authors":"Yicun Liu, Xi Luo, WeiJie Chen, Zhixing Dong, Tiaochun Cheng, Lin Chen, Linling Ju, Weihua Cai, Zhaolian Bian","doi":"10.1080/15384101.2024.2345469","DOIUrl":"10.1080/15384101.2024.2345469","url":null,"abstract":"Circular RNA (circRNA) can influence the development of hepatocellular carcinoma (HCC) as a competitive endogenous RNA (ceRNA). However, there are still many circRNAs whose functions are unknown. Our research explores the role of a novel circRNA, hsa_circ_0079875, in HCC. The expression of hsa_circ_0079875 in HCC was verified by next-generation sequencing, quantitative reverse transcription-polymerase chain reaction (qRT-PCR), and fluorescence in situ hybridization (FISH). The distribution of hsa_circ_0079875 in HCC cells was investigated by RNA subcellular isolation and FISH assays. The functional effects on HCC proliferation, invasion, migration, cell cycle, and apoptosis were verified by overexpression and knockdown of hsa_circ_0079875. Moreover, xenograft mouse models and immunohistochemistry experiments were used to assess the function of hsa_circ_0079875 in vivo. Hsa_circ_0079875 was up-regulated in HCC tissues and mainly distributed in the cytoplasm. Higher hsa_circ_0079875 leads to larger tumor tissue, more microvascular invasion(MVI) and higher AFP levels, which in turn leads to a poor prognosis. Overexpression of hsa_circ_0079875 can promote the proliferation, migration, and invasion of HCC cells and inhibit apoptosis in vitro and in vivo. Knocking down hsa_circ_0079875 has the opposite effect. Sequencing and biological information predicted the target miRNA and mRNA of hsa_circ_0079875. Further bioinformatics and clinical correlation analysis revealed that hsa_circ_0079875 promote the malignant biological behaviors of HCC through hsa_circ_0079875/miR-519d-59/NRAS ceRNA net. Therefore, hsa_circ_0079875 can be a potential prognostic marker and therapeutic target for HCC.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11135875/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140849480","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

MyoD1 promotes the transcription of BIK and plays an apoptosis-promoting role in the development of gastric cancer. MyoD1 可促进 BIK 的转录，并在胃癌的发展过程中发挥促进凋亡的作用。

IF 4.3 3区生物学

Cell Cycle Pub Date : 2024-03-01 Epub Date: 2024-05-03 DOI: 10.1080/15384101.2024.2348344

Fei Wu, Jinyuan Zhang, Qiuyu Jiang, Qian Li, Fang Li, Jia Li, Wei Lv, Xiaofei Wang, Yannan Qin, Chen Huang, Shuqun Zhang

{"title":"MyoD1 promotes the transcription of BIK and plays an apoptosis-promoting role in the development of gastric cancer.","authors":"Fei Wu, Jinyuan Zhang, Qiuyu Jiang, Qian Li, Fang Li, Jia Li, Wei Lv, Xiaofei Wang, Yannan Qin, Chen Huang, Shuqun Zhang","doi":"10.1080/15384101.2024.2348344","DOIUrl":"10.1080/15384101.2024.2348344","url":null,"abstract":"Myogenic differentiation (MyoD) 1, which is known as a pivotal transcription factor during myogenesis, has been proven dysregulated in several cancers. However, litter is known about the precise role and downstream genes of MyoD1 in gastric cancer (GC) cells. Here, we report that MyoD1 is lowly expressed in primary GC tissues and cells. In our experiments, overexpression of MyoD1 inhibited cell proliferation. Downstream genes of MyoD1 regulation were investigated using RNA-Seq. As a result, 138 up-regulated genes and 20 down-regulated genes and 27 up-regulated lncRNAs and 20 down-regulated lncRNAs were identified in MyoD1 overexpressed MKN-45 cells, which participated in epithelial cell signaling in Helicobacter pylori infection, glycosaminoglycan biosynthesis (keratan sulfate), notch signaling pathway, and others. Among these genes, BIK was directly regulated by MyoD1 in GC cells and inhibited cancer cell proliferation. The BIK knockdown rescued the effects of MyoD1 overexpression on GC cells. In conclusion, MyoD1 inhibited cell proliferation via 158 genes and 47 lncRNAs downstream directly or indirectly that participated in multiple signaling pathways in GC, and among these, MyoD1 promotes BIK transcription by binding to its promoter, then promotes BIK-Bcl2-caspase 3 axis and regulates GC cell apoptosis.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11135814/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140862273","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

Gene expression profile of mitogen-activated kinases and microRNAs controlling their expression in HaCaT cell culture treated with lipopolysaccharide A and cyclosporine A. 经脂多糖 A 和环孢素 A 处理的 HaCaT 细胞培养过程中，丝裂原活化激酶的基因表达谱以及控制其表达的 microRNAs。

IF 4.3 3区生物学

Cell Cycle Pub Date : 2024-03-01

Michał Wójcik, Nikola Zmarzły, Alicja Derkacz, Tomasz Kulpok-Bagiński, Natasza Blek, Beniamin Oskar Grabarek

{"title":"Gene expression profile of mitogen-activated kinases and microRNAs controlling their expression in HaCaT cell culture treated with lipopolysaccharide A and cyclosporine A.","authors":"Michał Wójcik, Nikola Zmarzły, Alicja Derkacz, Tomasz Kulpok-Bagiński, Natasza Blek, Beniamin Oskar Grabarek","doi":"","DOIUrl":"","url":null,"abstract":"Studies indicate that mitogen-activated protein kinases (MAPKs) are activated and overexpressed in psoriatic lesions. The aim of the study was to assess changes in the expression pattern of genes encoding MAPKs and microRNA (miRNA) molecules potentially regulating their expression in human adult low-calcium high-temperature (HaCaT) keratinocytes exposed to bacterial lipopolysaccharide A (LPS) and cyclosporine A (CsA). HaCaT cells were treated with 1 µg/mL LPS for 8 h, followed by treatment with 100 ng/mL cyclosporine A for 2, 8, or 24 h. Untreated cells served as controls. The molecular analysis consists of microarray, quantitative real-time polymerase chain reaction, and enzyme-linked immunosorbent assay analyses. The statistical analysis of the obtained results was performed using Transcriptome Analysis Console and STATISTICA 13.5 PL with the statistical significance threshold of p < 0.05. Changes in the expression profile of six mRNAs: dual-specificity phosphatase 1 (DUSP1), dual-specificity phosphatase 4 (DUSP4), mitogen-activated protein kinase kinase 2 (MAP2K2), mitogen-activated protein kinase kinase 7 (MAP2K7), mitogen-activated protein kinase kinase kinase 2 (MAP3K2) and mitogen-activated protein kinase 9 (MAPK9) in cell culture exposed to LPS or LPS and the drug compared to the control. We observed that under the LPS and cyclosporine treatment, the expression o/ miR-34a, miR-1275, miR-3188, and miR-382 changed significantly (p < 0.05). We demonstrated a potential relationship between DUSP1 and miR-34a; DUSP4 and miR-34a, miR-382, and miR-3188; MAPK9 and miR-1275, MAP2K7 and mir-200-5p; MAP3K2 and mir-200-5p, which may be the subject of further research in the context of psoriasis.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140038820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

NCAPD2 promotes the malignant progression of oral squamous cell carcinoma via the Wnt/β-catenin pathway. NCAPD2 通过 Wnt/β-catenin 通路促进口腔鳞状细胞癌的恶性发展。

IF 4.3 3区生物学

Cell Cycle Pub Date : 2024-03-01 Epub Date: 2024-05-14 DOI: 10.1080/15384101.2024.2348918

Ping Ma, Huajiao Yu, Mingda Zhu, Li Liu, Luyao Cheng, Zhengxue Han, Wulong Jin

{"title":"NCAPD2 promotes the malignant progression of oral squamous cell carcinoma via the Wnt/β-catenin pathway.","authors":"Ping Ma, Huajiao Yu, Mingda Zhu, Li Liu, Luyao Cheng, Zhengxue Han, Wulong Jin","doi":"10.1080/15384101.2024.2348918","DOIUrl":"10.1080/15384101.2024.2348918","url":null,"abstract":"Oral squamous cell carcinoma (OSCC) is the most common type of oral cancer, with a poor prognosis, yet the underlying mechanism needs further exploration. Non-SMC condensin I complex subunit D2 (NCAPD2) is a widely expressed protein in OSCC, but its role in tumor development is unclear. This study aimed to explore NCAPD2 expression and its biological function in OSCC. NCAPD2 expression in OSCC cell lines and tissue specimens was analyzed using quantitative polymerase chain reaction, western blotting, and immunohistochemistry. Cancer cell growth was evaluated using cell proliferation, 5-Ethynyl-2'-deoxyuridine (EdU) staining, and colony formation assays. Cell migration was evaluated using wound healing and Transwell assays. Apoptosis was detected using flow cytometry. The influence of NCAPD2 on tumor growth in vivo was evaluated in a mouse xenograft model. NCAPD2 expression was significantly higher in OSCC than that in normal oral tissue. In vitro, the knockdown of NCAPD2 inhibited OSCC cell proliferation and promoted apoptosis. NCAPD2 depletion also significantly inhibited the migration of OSCC cells. Moreover, NCAPD2 overexpression induced inverse effects on OSCC cell phenotypes. In vivo, we demonstrated that downregulating NCAPD2 could inhibit the tumorigenicity of OSCC cells. Mechanically, OSCC regulation by NCAPD2 involved the Wnt/β-catenin signaling pathway. These results suggest NCAPD2 as a novel oncogene with an important role in OSCC development and a candidate therapeutic target for OSCC.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11135826/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140921099","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

UHRF2 accumulates in early G₁-phase after serum stimulation or mitotic exit to extend G₁ and total cell cycle length. UHRF2 在血清刺激或有丝分裂结束后的 G1 期早期积累，从而延长 G1 期和细胞周期的总长度。

IF 4.3 3区生物学

Cell Cycle Pub Date : 2024-03-01 Epub Date: 2024-05-16 DOI: 10.1080/15384101.2024.2353553

Xiaohong Wang, Huarui Lu, Grace Sprangers, Timothy C Hallstrom

{"title":"UHRF2 accumulates in early G1-phase after serum stimulation or mitotic exit to extend G1 and total cell cycle length.","authors":"Xiaohong Wang, Huarui Lu, Grace Sprangers, Timothy C Hallstrom","doi":"10.1080/15384101.2024.2353553","DOIUrl":"10.1080/15384101.2024.2353553","url":null,"abstract":"Ubiquitin like with PHD and ring finger domains 2 (UHRF2) regulates the cell cycle and epigenetics as a multi-domain protein sharing homology with UHRF1. UHRF1 functions with DNMT1 to coordinate daughter strand methylation during DNA replication, but UHRF2 can't perform this function, and its roles during cell cycle progression are not well defined. UHRF2 role as an oncogene vs. tumor suppressor differs in distinct cell types. UHRF2 interacts with E2F1 to control Cyclin E1 (CCNE1) transcription. UHRF2 also functions in a reciprocal loop with Cyclin E/CDK2 during G1, first as a direct target of CDK2 phosphorylation, but also as an E3-ligase with direct activity toward both Cyclin E and Cyclin D. In this study, we demonstrate that UHRF2 is expressed in early G1 following either serum stimulation out of quiescence or in cells transiting directly out of M-phase, where UHRF2 protein is lost. Further, UHRF2 depletion in G2/M is reversed with a CDK1 specific inhibitor. UHRF2 controls expression levels of cyclins and CDK inhibitors and controls its own transcription in a negative-feedback loop. Deletion of UHRF2 using CRISPR/Cas9 caused a delay in passage through each cell cycle phase. UHRF2 loss culminated in elevated levels of cyclins but also the CDK inhibitor p27KIP1, which regulates G1 passage, to reduce retinoblastoma phosphorylation and increase the amount of time required to reach G1/S passage. Our data indicate that UHRF2 is a central regulator of cell-cycle pacing through its complex regulation of cell cycle gene expression and protein stability.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11135863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140944123","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

Pseudogene OCT4-pg5 upregulates OCT4B expression to promote bladder cancer progression by competing with miR-145-5p. 伪基因OCT4-pg5通过与miR-145-5p竞争，上调OCT4B的表达，从而促进膀胱癌的进展。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2024-03-01 Epub Date: 2024-06-06 DOI: 10.1080/15384101.2024.2353554

Wuer Zhou, Yue Yang, Wei Wang, Chenglin Yang, Zhi Cao, Xiaoyu Lin, Huifen Zhang, Yuansong Xiao, Xiaoming Zhang

{"title":"Pseudogene OCT4-pg5 upregulates OCT4B expression to promote bladder cancer progression by competing with miR-145-5p.","authors":"Wuer Zhou, Yue Yang, Wei Wang, Chenglin Yang, Zhi Cao, Xiaoyu Lin, Huifen Zhang, Yuansong Xiao, Xiaoming Zhang","doi":"10.1080/15384101.2024.2353554","DOIUrl":"10.1080/15384101.2024.2353554","url":null,"abstract":"Bladder cancer (BC) is one of the most common malignant neoplasms worldwide. Competing endogenous RNA (ceRNA) networks may identify potential biomarkers associated with the progression and prognosis of BC. The OCT4-pg5/miR-145-5p/OCT4B ceRNA network was found to be related to the progression and prognosis of BC. OCT4-pg5 expression was significantly higher in BC cell lines than in normal bladder cells, with OCT4-pg5 expression correlating with OCT4B expression and advanced tumor grade. Overexpression of OCT4-pg5 and OCT4B promoted the proliferation and invasion of BC cells, whereas miR-145-5p suppressed these activities. The 3' untranslated region (3'UTR) of OCT4-pg5 competed for miR-145-5p, thereby increasing OCT4B expression. In addition, OCT4-pg5 promoted epithelial-mesenchymal transition (EMT) by activating the Wnt/β-catenin pathway and upregulating the expression of matrix metalloproteinases (MMPs) 2 and 9 as well as the transcription factors zinc finger E-box binding homeobox (ZEB) 1 and 2. Elevated expression of OCT4-pg5 and OCT4B reduced the sensitivity of BC cells to cisplatin by reducing apoptosis and increasing the proportion of cells in G1. The OCT4-pg5/miR-145-5p/OCT4B axis promotes the progression of BC by inducing EMT via the Wnt/β-catenin pathway and enhances cisplatin resistance. This axis may represent a therapeutic target in patients with BC.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11229759/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141261382","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

Surfeit locus protein 4 modulates endoplasmic reticulum function and maintains oocyte quality. 过剩基因座蛋白 4 可调节内质网功能并保持卵母细胞质量。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2024-03-01 Epub Date: 2024-05-31 DOI: 10.1080/15384101.2024.2360287

Yuanyuan Li, Li-Quan Zhou, Ying Yin

引用次数: 0