Cell CyclePub Date : 2024-03-28DOI: 10.1080/15384101.2024.2335024
Jie Tang, Song Li, Zixiao Zhou, Weicai Chang, Yongqiang Wang, Juan Mei, Shaobo Zhou
{"title":"Identification and validation of key miRNAs and a microRNA-mRNA regulatory network associated with liver cancer","authors":"Jie Tang, Song Li, Zixiao Zhou, Weicai Chang, Yongqiang Wang, Juan Mei, Shaobo Zhou","doi":"10.1080/15384101.2024.2335024","DOIUrl":"https://doi.org/10.1080/15384101.2024.2335024","url":null,"abstract":"MiRNAs play crucial regulatory roles in the growth and development of tumor cells by serving as carriers of post-transcriptional regulatory information derived from genes. Investigating the potenti...","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"44 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140314421","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}
Cell CyclePub Date : 2024-03-21DOI: 10.1080/15384101.2024.2330225
Yuping Yan, Xiaoyan Du, Xia Dou, Jingjie Li, Wenjie Zhang, Shuangyu Yang, Wenting Meng, Gang Tian
{"title":"Effects of Ninjurin 2 polymorphisms on susceptibility to coronary heart disease","authors":"Yuping Yan, Xiaoyan Du, Xia Dou, Jingjie Li, Wenjie Zhang, Shuangyu Yang, Wenting Meng, Gang Tian","doi":"10.1080/15384101.2024.2330225","DOIUrl":"https://doi.org/10.1080/15384101.2024.2330225","url":null,"abstract":"The aim of this study was to explore the effects of Ninjurin 2 (NINJ2) polymorphisms on susceptibility to coronary heart disease (CHD).We conducted a case-control study with 499 CHD cases and 505 a...","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"158 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140204677","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}
Cell CyclePub Date : 2024-03-06DOI: 10.1080/15384101.2024.2320508
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":"10.1080/15384101.2024.2320508","DOIUrl":"https://doi.org/10.1080/15384101.2024.2320508","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 e...","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"56 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140070744","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}
Cell CyclePub Date : 2024-03-01Epub Date: 2024-05-02DOI: 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":"<p><p>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 <i>TGF-β-1</i> and <i>TGF-β-3</i>, while <i>TGF-β-2</i> 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; <i>p</i> < 0.0001), TGF-β-2 (3104.34 pg/mL ± 1192.74 pg/mL vs. 258.86 pg/mL ± 82.98 pg/mL; <i>p</i> < 0.0001), TGF-β-3 (512.75 pg/mL ± 107.36 pg/mL vs. 55.06 pg/mL ± 9.83 pg/mL, <i>p</i> < 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.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"555-572"},"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}
Cell CyclePub Date : 2024-03-01Epub Date: 2024-06-12DOI: 10.1080/15384101.2024.2357909
Dongli Zhang, Yan Zhou, Chenyang Jiao, Hongfang Kong, Zhibin Zhao, Yujiang Li
{"title":"Circ_0050444 represses esophageal squamous cell carcinoma progression through sponging miR-486-3p to upregulate C10orf91.","authors":"Dongli Zhang, Yan Zhou, Chenyang Jiao, Hongfang Kong, Zhibin Zhao, Yujiang Li","doi":"10.1080/15384101.2024.2357909","DOIUrl":"10.1080/15384101.2024.2357909","url":null,"abstract":"<p><p>Esophageal squamous cell carcinoma (ESCC) ranks as the fourth leading cause of tumor-related deaths in China. Circ_0050444 has been revealed to be downregulated in ESCC tissues, however, its function and molecular mechanism underlying ESCC progression is unknown. Therefore, we attempted to clarify the functional role and molecular mechanism of circ_0050444 underlying ESCC progression. RT-qPCR and RNase R digestion assays were used to evaluate circ_0050444 expression and stability characteristics in ESCC cells. Gain-of-function assays were conducted to clarify circ_0050444 role in ESCC cell malignant behaviors. Bioinformatics and mechanism experiments were performed to assess the relationship between circ_0050444 or C10orf91 and miR-486-3p in ESCC cells. Rescue assays were conducted to evaluate the regulatory function of the circ_0050444-miR-486-3p-C10orf91 axis in ESCC cellular processes. Circ_0050444 expression was found to be downregulated both in ESCC patient tissues and cell lines. Functionally, circ_0050444 overexpression repressed ESCC cell proliferative, migratory, and invasive capabilities in cultured cells. Mechanistically, circ_0050444 was found to be competitively bound with miR-486-3p to upregulate C10orf91 in ESCC cells. Moreover, the impact of circ_0050444 elevation on ESCC cell proliferation, migration, and invasion was countervailed by C10orf91 silencing. Circ_0050444 presents downregulation and functions as a tumor suppressor in ESCC progression. Circ_0050444 suppresses ESCC proliferation, migration, and invasion through sponging miR-486-3p to upregulate C10orf91, providing a potential new direction for seeking therapeutic plans for ESCC.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"693-702"},"PeriodicalIF":3.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11229726/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141310143","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}
{"title":"Exploring the multifaceted role of RASGRP1 in disease: immune, neural, metabolic, and oncogenic perspectives.","authors":"Shangzhi Fan, Bo Kang, Shaoqian Li, Weiyi Li, Canyu Chen, Jixiang Chen, Lijing Deng, Danjun Chen, Jiecan Zhou","doi":"10.1080/15384101.2024.2366009","DOIUrl":"10.1080/15384101.2024.2366009","url":null,"abstract":"<p><p>RAS guanyl releasing protein 1 (RASGRP1) is a guanine nucleotide exchange factor (GEF) characterized by the presence of a RAS superfamily GEF domain. It functions as a diacylglycerol (DAG)-regulated nucleotide exchange factor, specifically activating RAS through the exchange of bound GDP for GTP. Activation of RAS by RASGRP1 has a wide range of downstream effects at the cellular level. Thus, it is not surprising that many diseases are associated with RASGRP1 disorders. Here, we present an overview of the structure and function of RASGRP1, its crucial role in the development, expression, and regulation of immune cells, and its involvement in various signaling pathways. This review comprehensively explores the relationship between RASGRP1 and various diseases, elucidates the underlying molecular mechanisms of RASGRP1 in each disease, and identifies potential therapeutic targets. This study provides novel insights into the role of RASGRP1 in insulin secretion and highlights its potential as a therapeutic target for diabetes. The limitations and challenges associated with studying RASGRP1 in disease are also discussed.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"722-746"},"PeriodicalIF":3.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11229727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141310144","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}
{"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":"<p><p>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.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"602-612"},"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}
Cell CyclePub Date : 2024-03-01Epub Date: 2024-05-24DOI: 10.1080/15384101.2024.2355825
Yang Yu, Gang Nie, Yi-Wei Ren, Liu Ouyang, Chen-Ming Ni
{"title":"Pumilio RNA binding family member 1 deficiency activates anti-tumor immunity in hepatocellular carcinoma via restraining M2 macrophage polarization.","authors":"Yang Yu, Gang Nie, Yi-Wei Ren, Liu Ouyang, Chen-Ming Ni","doi":"10.1080/15384101.2024.2355825","DOIUrl":"10.1080/15384101.2024.2355825","url":null,"abstract":"<p><p>Pumilio RNA-binding family member 1 (PUM1) has been implicated in both the progression of colorectal cancer and the regulation of inflammation. The role of PUM1 in the polarization of tumor-associated macrophages (TAMs) into the M2 phenotype has not yet been reported in hepatocellular carcinoma. Using the PUM1-knockout mice model, flow cytometry, and IHC, we validated the role of PUM1 in hepatocellular carcinoma (HCC) TAMs. One-way analysis of variance (ANOVA) or student's t-tests was used to compare the experimental groups. We found that PUM1 inhibited anti-tumor immunity in HCC through TAM-mediated inhibition of CD8+ T cells. We also showed that PUM1 promotes the transformation of TAMs into pro-tumorigenic M2-like phenotypes by activating cAMP signaling pathway. This study emphasized the potential of PUM1 as a target for immunotherapy in HCC through TAMs. The present study revealed the molecular mechanism underlying the pro-tumor role of PUM1 in HCC.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"682-692"},"PeriodicalIF":3.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11229713/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141093076","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}
Cell CyclePub Date : 2024-03-01Epub Date: 2024-04-29DOI: 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":"<p><p>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 <i>in vivo</i>. 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 <i>in</i> <i>vitro and in</i> <i>vivo</i>. 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.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"519-536"},"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}
{"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":"<p><p>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.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"573-587"},"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}