Critical Reviews in Eukaryotic Gene Expression最新文献

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Multi-Omics Analysis of the Prognostic and Immunological Role of Runt-Related Transcription Factor 3 in Pan-Cancer. 多指标分析 Runt 相关转录因子 3 在泛癌症中的预后和免疫作用
IF 1.6 4区 医学
Critical Reviews in Eukaryotic Gene Expression Pub Date : 2023-01-01 DOI: 10.1615/CritRevEukaryotGeneExpr.2023044081
Quan Zhou, Dou-Dou Ding, Man Lu, Man-Zhen Zuo
{"title":"Multi-Omics Analysis of the Prognostic and Immunological Role of Runt-Related Transcription Factor 3 in Pan-Cancer.","authors":"Quan Zhou, Dou-Dou Ding, Man Lu, Man-Zhen Zuo","doi":"10.1615/CritRevEukaryotGeneExpr.2023044081","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2023044081","url":null,"abstract":"<p><p>Runt-related transcription factor 3 (RUNX3) plays a pivotal role in tumor microenvironment and immune infiltration. However, the prognostic and immunological roles of RUNX3 in pancancer remain unclear. In the current study, we explored the expression profiles, prognostic landscape, and immune infiltration of RUNX3 in pancancer through a variety of online platforms, including HPA, ONCOMINE, UALCAN, GEPIA, PrognoScan, TCGA, TIMER, R2, and Reactome databases. In general, RUNX3 was widely expressed in tonsil, gallbladder, skin, spleen, lymph node, and bone marrow, and RUNX3 was frequently higher expression in tumor tissues compared to normal tissues. In prognostic analysis, the RUNX3 expression level was significantly correlated with the clinical outcomes of bladder cancer, blood cancer, brain cancer, breast cancer, colorectal cancer, lung cancer, and ovarian cancer. In mutation analysis, a total 72 mutation sites were located within amino acids 1 to 415 of RUNX3, including 65 missense sites and seven truncating sites, whereas the mutation frequency of skin cutaneous melanoma and uterine corpus endometrial carcinoma (UCEC) is relatively high (> 3%). In immune infiltration analysis, the RUNX3 expression level was significantly related to recognized markers and the immune infiltration levels of various types of immune cells in colon adenocarcinoma (COAD) and brain lower grade glioma (LGG). After that, 453 RUNX3 co-expressed genes were recognized in COAD, lymphoid neoplasm diffuse large B-cell lymphoma, LGG, and ovarian serous cystadenocarcinoma (OV). Pathway enrichment analysis revealed that RUNX3 co-expressed genes were remarkably enriched in immune system and tumor progression pathways. RUNX3 expression is associated with clinical prognosis, immune infiltration, and identified RUNX3 related pathways in a variety of tumors, which may serve as targets of promising prognostic markers and novel therapeutic targets for various human cancers.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"33 4","pages":"63-83"},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9501739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Novel pathways between invasiveness modulators in breast cancer single cells 乳腺癌单细胞侵袭性调节因子之间的新途径
4区 医学
Critical Reviews in Eukaryotic Gene Expression Pub Date : 2023-01-01 DOI: 10.1615/critreveukaryotgeneexpr.2023050843
George Eliceiri
{"title":"Novel pathways between invasiveness modulators in breast cancer single cells","authors":"George Eliceiri","doi":"10.1615/critreveukaryotgeneexpr.2023050843","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2023050843","url":null,"abstract":"Individual cells are known to behave differently than their whole populations of cells. The present work focused on proteins that control cancer invasiveness. Individual Dicer siRNA knockdown of HER4, CDC42, and E-cadherin decreased MMP1 mRNA levels in SCP2, a cancer single-cell progeny that is highly metastatic to bone and adrenal gland. Individual knockdown of β-catenin, CDC42, HER3, and the γ catalytic subunit of PI3K raised MMP1 mRNA levels in SCP21, a single-cell progeny of the same tumor and patient, with low metastasis to bone and adrenal.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"6 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":"135506663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Hsa_circ_0007334 Promotes the Osteogenic Differentiation and Proliferation of Human Bone Marrow Mesenchymal Stem Cells by Sponging miR-144-3p. Hsa_circ_0007334通过海绵miR-144-3p促进人骨髓间充质干细胞成骨分化和增殖
IF 1.6 4区 医学
Critical Reviews in Eukaryotic Gene Expression Pub Date : 2023-01-01 DOI: 10.1615/CritRevEukaryotGeneExpr.2022044929
Meng-Jun Liu, Bin Du, Jin-Song Yu, Ji Zhao, Hao Chen, Xing-Sheng Xiang, Yu-Zhu Wang, Wei Chen
{"title":"Hsa_circ_0007334 Promotes the Osteogenic Differentiation and Proliferation of Human Bone Marrow Mesenchymal Stem Cells by Sponging miR-144-3p.","authors":"Meng-Jun Liu,&nbsp;Bin Du,&nbsp;Jin-Song Yu,&nbsp;Ji Zhao,&nbsp;Hao Chen,&nbsp;Xing-Sheng Xiang,&nbsp;Yu-Zhu Wang,&nbsp;Wei Chen","doi":"10.1615/CritRevEukaryotGeneExpr.2022044929","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2022044929","url":null,"abstract":"<p><p>This study aimed to identify the possible function and the molecular mechanism of hsa_circ_0007334 in human bone marrow mesenchymal stem cells (hBMSCs) osteogenic differentiation. The level of hsa_circ_0007334 was detected by means of quantitative real-time polymerase chain reaction (RT-qPCR). Alkaline phosphatase (ALP), RUNX2, osterix (OSX), and osteocalcin (OCN) were monitored to analyze the degree of osteogenic differentiation under routine culture or under the control of hsa_circ_0007334. The proliferation of hBMSCs was tested with a cell counting kit-8 (CCK-8) assay. The migration of hBMSCs was tested using the Transwell assay. Bioinformatics analysis was used to predict the possible targets of hsa_circ_0007334 or miR-144-3p. Dual-luciferase reporter assay system was used to analyze the combination between hsa_circ_0007334 and miR-144-3p. Hsa_circ_0007334 was upregulated in osteogenic differentiation of hBMSCs. Osteogenic differentiation increased by hsa_circ_0007334 in vitro was confirmed with levels of ALP and bone markers (RUNX2, OCN, OSX). hsa_circ_0007334 overexpression promoted osteogenic differentiation, proliferation, and migration of hBMSCs, and knockdown of hsa_circ_0007334 has the opposite effects. miR-144-3p was identified as the target of hsa_circ_0007334. The targeting genes of miR-144-3p are involved in osteogenic-differentia-tion-related biological processes (such as bone development, epithelial cell proliferation, and mesenchymal cell apoptotic prosess) and pathways (including FoxO and VEGF signaling pathway). Hsa_circ_0007334, therefore, presents itself as a promising biological for osteogenic differentiation.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"33 3","pages":"61-70"},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9275430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
hsa_circ_0051428 Facilitates the Progression of Thyroid Cancer by Sponging miR-1248 to Up-Regulate FN1. hsa_circ_0051428通过海绵miR-1248上调FN1促进甲状腺癌的进展。
IF 1.6 4区 医学
Critical Reviews in Eukaryotic Gene Expression Pub Date : 2023-01-01 DOI: 10.1615/CritRevEukaryotGeneExpr.2022044777
Tao Zhou, Yuanyuan Zhang, Shilin Zheng, Fuhua Wang, Shengpan Jiang, Wenfeng Lei, Lili Xu, Yiqing Tan
{"title":"hsa_circ_0051428 Facilitates the Progression of Thyroid Cancer by Sponging miR-1248 to Up-Regulate FN1.","authors":"Tao Zhou,&nbsp;Yuanyuan Zhang,&nbsp;Shilin Zheng,&nbsp;Fuhua Wang,&nbsp;Shengpan Jiang,&nbsp;Wenfeng Lei,&nbsp;Lili Xu,&nbsp;Yiqing Tan","doi":"10.1615/CritRevEukaryotGeneExpr.2022044777","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2022044777","url":null,"abstract":"<p><p>Evidence displays that circular RNAs (circRNAs) are considerable mediators of numerous processes in cancer development. Given that many circRNAs are not functionally characterized, our aim was to explore the function and mechanisms of circ_0051428 in thyroid cancer (TC). The analysis of circ_0051428, miR-1248 and FN1 mRNA expression was conducted using real-time quantitative polymerase chain reaction. Cell growth was observed using CCK-8 and colony formation assays. Cell migration was investigated using wound healing assay. Cell apoptosis was identified by the expression of apoptosis-related proteins (Bax and Bcl-2) using Western blotting. Animal models were established to testify the role of circ_0051428 in vivo. The assumed binding between miR-1248 and circ_0051428 or FN1 was identified using dual-luciferase reporter or RIP assay. circ_0051428 exhibits an abnormally elevated expression in TC. circ_0051428 deficiency caused inhibition of TC cell proliferation, migration, clonogenic capacity, and inhibition of tumor growth in vivo. circ_0051428 directly targeted miR-1248, and FN1 was a target downstream of circ_0051428/miR-1248 axis. circ_0051428 could sponge miR-1248 to upregulate FN1. Furthermore, miR-1248 downregulation recovered circ_0051428 deficiency-suppressed cancer cell proliferation, survival and migration. Besides, the repressive effects of FN1 knockdown on cancer cell growth, survival and migration were also partly abolished by miR-1248 downregulation. circ_0051428 targeted miR-1248 to modulate FN1 expression, thereby facilitating the malignant progression of TC, which contributed to the understanding of the molecular mechanism of TC development.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"33 4","pages":"25-38"},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9495303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
KIF20B correlates with LUAD progression and is an independent risk factor KIF20B与LUAD进展相关,是一个独立的危险因素
4区 医学
Critical Reviews in Eukaryotic Gene Expression Pub Date : 2023-01-01 DOI: 10.1615/critreveukaryotgeneexpr.2023050271
Jianye Yang, Liang Xu, Xiaoliang Han
{"title":"KIF20B correlates with LUAD progression and is an independent risk factor","authors":"Jianye Yang, Liang Xu, Xiaoliang Han","doi":"10.1615/critreveukaryotgeneexpr.2023050271","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2023050271","url":null,"abstract":"Objective: Kinesin family proteins (KIFs) play crucial roles in human tumorigenesis and progression. This study aimed to investigate the expression and association of Kinesin family member 20B (KIF20B) with lung adenocarcinoma (LUAD). Methods: RNA-seq data from LUAD patients (n=535) were extracted from TCGA. KIF20B expression was compared between tumor tissues and controls, and between different stages of the disease. Survival and Cox regression analyses were performed, as well as in vitro cellular experiments on A549 cells. Results: KIF20B is upregulated in LUAD tumor tissues compared with controls and is higher in advanced stages. Patients with high expression of KIF20B have shorter survival times. KIF20B is an independent risk factor for the prognosis of LUAD. High KIF20B expression samples were enriched in signaling pathways related to tumor progression. si-KIF20B transfection reduced migration and invasion of A549 cells and increased apoptosis. The expression of p53 and Bax proteins were upregulated by si-KIF20B, while Bcl-2 was down-regulated. Discussion: This study reveals that high KIF20B expression is an independent risk factor for the poor prognosis of LUAD. The inhibition of KIF20B might be of great value for suppressing LUAD progression.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","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":"135267583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Identification of a Diagnosis and Therapeutic Inflammatory Response-Related Gene Signature Associated with Esophageal Adenocarcinoma. 与食管腺癌相关的诊断和治疗炎症反应相关基因特征的鉴定。
IF 1.6 4区 医学
Critical Reviews in Eukaryotic Gene Expression Pub Date : 2023-01-01 DOI: 10.1615/CritRevEukaryotGeneExpr.2023048608
Yang Xie, Jun Li, Qing Tao, Chunyan Zeng, Youxiang Chen
{"title":"Identification of a Diagnosis and Therapeutic Inflammatory Response-Related Gene Signature Associated with Esophageal Adenocarcinoma.","authors":"Yang Xie,&nbsp;Jun Li,&nbsp;Qing Tao,&nbsp;Chunyan Zeng,&nbsp;Youxiang Chen","doi":"10.1615/CritRevEukaryotGeneExpr.2023048608","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2023048608","url":null,"abstract":"<p><p>The purpose of this study is to identify the key regulatory genes related to the inflammatory response of esophageal adenocarcinoma (EAC) and to find new diagnosis and therapeutic options. We downloaded the dataset GSE72874 from the Gene Expression Omnibus database for this study. Weighted gene co-expression network analysis (WGCNA) and differentially expressed genes (DEGs) analysis were used to find common inflammatory response-related genes (IRRGs) in EAC. The relationship between normal and tumor immune infiltration was analyzed using an online database of CIBERSORTx. Finally, 920 DEGs were identified, of which 5 genes were key IRRGs associated with EAC, including three down-regulated genes GNA15, MXD1, and NOD2, and two down-regulated genes PLAUR and TIMP1. Further research found that GNA15, MXD1, and NOD2 were down-regulated, PLAUR and TIMP1 were up-regulated in Barrett's esophagus (BE). In addition, we found that the expression of GNA15 and MXD1 in normal esophageal squamous epithelial cells decreased after ethanol treatment, while the expression of PLAUR and TIMP1 increased after ethanol treatment. Compared with normal esophageal tissue, immune cells infiltrated such as plasma cells, macrophages M0, macrophages M1, macrophages M2, dendritic cells activated, and mast cells activated were significantly increased in EAC, while immune cells infiltrated such as T cells CD4 memory resting, T cells follicular helper, NK cells resting, and dendritic cells resting were significantly reduced. The receiver operating characteristic curve indicated that GNA15, MXD1, NOD2, PLAUR and TIMP1 expression had a performed well in diagnosing EAC from healthy control. GNA15, MXD1, NOD2, PLAUR and TIMP1 were identified and validated as novel potential biomarkers for early diagnosis and may be new molecular targets for treatment of EAC.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"33 7","pages":"65-80"},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10425358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
IncRNA MIAT Accelerates Keloid Formation by miR-411-5p/JAG1 Axis. IncRNA MIAT通过miR-411-5p/JAG1轴加速瘢痕疙瘩形成。
IF 1.6 4区 医学
Critical Reviews in Eukaryotic Gene Expression Pub Date : 2023-01-01 DOI: 10.1615/CritRevEukaryotGeneExpr.2022044734
Yingyan Yu, Yujie Dong, Benyuan Deng, Ting Yang
{"title":"IncRNA MIAT Accelerates Keloid Formation by miR-411-5p/JAG1 Axis.","authors":"Yingyan Yu,&nbsp;Yujie Dong,&nbsp;Benyuan Deng,&nbsp;Ting Yang","doi":"10.1615/CritRevEukaryotGeneExpr.2022044734","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2022044734","url":null,"abstract":"<p><p>The long non-coding RNA (lncRNA) myocardial infarction-associated transcript (MIAT) regulates the biological functions of many kinds of cells. The aim of this study is to explore the mechanism of MIAT and how it affects keloid progression. The expressions of MIAT, JAG1, and miR-411-5p in keloid tissues and keloid fibroblasts (KEL FIBs) were quantified by conducting Western blot and quantitative reverse transcription polymerase chain reaction analyses. The influences of MIAT, JAG1, and miR-411-5p on the abilities of KEL FIBs to proliferate, migrate, and invade were assessed by means of the CCK-8, wound healing, and Transwell experiments. To determine the binding relationship among MIAT, JAG1, and miR-411-5p, we performed luciferase reporter and RIP experiments. In keloid tissues and KEL FIBs, MIAT and JAG1 were upregulated while miR-411-5p was downregulated. Knocking-down MIAT or JAG1 significantly inhibited proliferation, migration and invasion. On the contrary, suppressing miR-411-5p expression produced an opposite effect. With regard to mechanisms, MIAT sponged miR-411-5p, which targeted JAG1. MIAT accelerates keloid formation by modulating the miR-411-5p/JAG1 axis.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"33 2","pages":"81-92"},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9634274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
linc00511 Knockdown Inhibits Lung Cancer Progression by Regulating miR-16-5p/MMP11. linc00511敲低通过调节miR-16-5p/MMP11抑制肺癌进展
IF 1.6 4区 医学
Critical Reviews in Eukaryotic Gene Expression Pub Date : 2023-01-01 DOI: 10.1615/CritRevEukaryotGeneExpr.2023047789
Zhengyi Song, Jing Luo, Ming Wu, Zelin Zhang
{"title":"linc00511 Knockdown Inhibits Lung Cancer Progression by Regulating miR-16-5p/MMP11.","authors":"Zhengyi Song,&nbsp;Jing Luo,&nbsp;Ming Wu,&nbsp;Zelin Zhang","doi":"10.1615/CritRevEukaryotGeneExpr.2023047789","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2023047789","url":null,"abstract":"<p><p>Lung cancer (LC) is a malignant tumor that extremely impairs people. According to numerous studies, long non-coding RNA (lncRNA) was inextricably involved in the advancement of LC. The work aspired to identify linc00511 expression in LC and to dig for the underlying mechanisms linc00511 regulated LC progression. Experimental outcomes revealed that linc00511 was obviously upregulated in LC, and linc00511 knockdown significantly impaired the malignant phenotype of LC cells in vitro. For an in-depth study on the contribution of linc00511 to LC advancement, it was disclosed that miR-16-5p had binding sites to the sequence of linc00511, which also inversely affected linc00511 expression in LC. Further experimental data demonstrated that miR-16-5p directly and negatively targeted matrix metallopeptidase 11 (MMP11). Also, rescue experiments displayed that miR-16-5p inhibition or MMP11 overexpressing offset the suppressive impacts of linc00511 silencing on LC progression. To sum up, our findings indicated that linc00511 performed a crucial role in facilitating LC progression, and mechanistic studies demonstrated that linc00511 aggravated LC progression via targeting the miR-16-5p/MMP11 axis.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"33 7","pages":"17-30"},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10050266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
MicroRNA-17 Family Targets RUNX3 to Increase Proliferation and Migration of Hepatocellular Carcinoma. MicroRNA-17家族靶向RUNX3增加肝细胞癌的增殖和迁移
IF 1.6 4区 医学
Critical Reviews in Eukaryotic Gene Expression Pub Date : 2023-01-01 DOI: 10.1615/critreveukaryotgeneexpr.2022043382
Xiaofei Wang, Fang Li, Jiwen Cheng, N. Hou, Zhiying Pu, Hua Zhang, Yanke Chen, Chen Huang
{"title":"MicroRNA-17 Family Targets RUNX3 to Increase Proliferation and Migration of Hepatocellular Carcinoma.","authors":"Xiaofei Wang, Fang Li, Jiwen Cheng, N. Hou, Zhiying Pu, Hua Zhang, Yanke Chen, Chen Huang","doi":"10.1615/critreveukaryotgeneexpr.2022043382","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2022043382","url":null,"abstract":"Hepatocellular carcinoma (HCC) is one common cancer in the world. Previous studies have shown that miR-17 family members are elevated in most tumors and promote tumor progression. However, there is no comprehensive analysis of the expression and functional mechanism of the microRNA-17 (miR-17) family in HCC. The aim of this study is to comprehensively analyze the function of the miR-17 family in HCC and the molecular mechanism of its role. Bioinfoimatics analysis of the miR-17 family expression profile and its relationship to clinical significance using The Cancer Genome Atlas (TCGA) database, and this result was confirmed using quantitative real-time polymerase chain reaction. miR-17 family members were tested for functional effects through transfection of miRNA precursors and inhibitors, and monitoring cell viability and migration by cell count and wound healing assays. In addition, we using dual-luciferase assay and Western blot demonstrated the targeting relationship between the miRNA-17 family and RUNX3. These members of miR-17 family were highly expressed in HCC tissues, and the overexpression of the miR-17 family promoted the proliferation and migration of SMMC-7721 cells, whereas treatment with anti-miR17 inhibitors caused the opposite effects. Notably, we also found that inhibitors anti-each member of miR-17 can suppress the expression of the entire family member. In addition, they can bind to the 3' untranslated region of RUNX3 to regulate its expression at the translational level. Our results proved that miR-17 family has oncogenic characteristics, overexpression every member of the family contributed to HCC cell proliferation and migration by reducing the translation of RUNX3.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"33 3 1","pages":"71-84"},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67424296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
IncRNA XIST Stimulates Papillary Thyroid Cancer Development through the miR-330-3p/PDE5A Axis. IncRNA XIST通过miR-330-3p/PDE5A轴刺激甲状腺乳头状癌的发展。
IF 1.6 4区 医学
Critical Reviews in Eukaryotic Gene Expression Pub Date : 2023-01-01 DOI: 10.1615/CritRevEukaryotGeneExpr.2022043844
Tao Cai, Yan He, Binyu Peng
{"title":"IncRNA XIST Stimulates Papillary Thyroid Cancer Development through the miR-330-3p/PDE5A Axis.","authors":"Tao Cai,&nbsp;Yan He,&nbsp;Binyu Peng","doi":"10.1615/CritRevEukaryotGeneExpr.2022043844","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2022043844","url":null,"abstract":"<p><p>Long non-coding RNAs (lncRNAs) possess both tumor suppressive and oncogenic functions in papillary thyroid cancer (PTC). Among all the thyroid cancers, PTC is the most prevalent form. Herein, we aim to determine the regulatory mechanisms and functions of lncRNA XIST in the multiplication, invasion, and survival of PTC. Quantitative reverse transcription polymerase chain reaction and Western blot experiments were performed to determine the patterns of lncRNA XIST, miR-330-3p, and PDE5A expressions. The subcellular localization of XIST was determined through subcellular fractionation. Bioinformatics analyses were performed to determine miR-330-3p's relationships with XIST and PDE5A, which were further confirmed through luciferase reporter assays. Loss-of-function combined with Transwell, CCK-8, and caspase-3 activity experiments were performed to determine the mechanism of the XIST/miR-330-3p/PDE5A axis in regulating the malignancy of PTC cells. Xenograft tumor experiment was employed to study the influence of XIST on tumor development in vivo. The PTC cell lines and tissues manifested considerably high levels of lncRNA XIST expression. The XIST knockdown inhibited proliferation, blocked migration, and strengthened apoptosis among PTC cells. Moreover, its knockdown suppressed PTC tumor development in vivo. XIST repressed miR-330-3p to stimulate the malignant behaviors of PTC. Through the downregulation of PDE5A, miR-330-3p attenuated the capability of PTC cells to grow, migrate, and survive. lncRNA XIST promotes tumor development in PTC through the regulation of the miR-330-3p/PDE5A axis. The findings from this study provide new insights into the treatment of PTC.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"33 3","pages":"13-26"},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9275432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
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