miR‑20b promotes cellular proliferation and migration by directly regulating phosphatase and tensin homolog in prostate cancer

Guo, Ju; Xiao, Zewen; Yu, Xingwei; Cao, Runfu

doi:10.3892/ol.2017.7041

Cited by 24 publications

(32 citation statements)

References 38 publications

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“…MiR-20b belongs to a cluster of highly similar miRNAs called the miR-17 family [22]. Deregulation of miR-20b has been determined in many different cancers [13][14][15][23][24][25][26]. Our results demonstrated that miR-20b is overexpressed in both AGS and MKN28 GC cell lines compared to healthy gastric tissue, which is consistent with previous studies [13,14,27,28].…”

Section: Discussionsupporting

confidence: 91%

miR-20b and miR-451a Are Involved in Gastric Carcinogenesis through the PI3K/AKT/mTOR Signaling Pathway: Data from Gastric Cancer Patients, Cell Lines and Ins-Gas Mouse Model

Streleckiene

Inčiūraitė

Juzėnas

et al. 2020

IJMS

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Gastric cancer (GC) is one of the most common and lethal gastrointestinal malignancies worldwide. Many studies have shown that development of GC and other malignancies is mainly driven by alterations of cellular signaling pathways. MicroRNAs (miRNAs) are small noncoding molecules that function as tumor-suppressors or oncogenes, playing an essential role in a variety of fundamental biological processes. In order to understand the functional relevance of miRNA dysregulation, studies analyzing their target genes are of major importance. Here, we chose to analyze two miRNAs, miR-20b and miR-451a, shown to be deregulated in many different malignancies, including GC. Deregulated expression of miR-20b and miR-451a was determined in GC cell lines and the INS-GAS mouse model. Using Western Blot and luciferase reporter assay we determined that miR-20b directly regulates expression of PTEN and TXNIP, and miR-451a: CAV1 and TSC1. Loss-of-function experiments revealed that down-regulation of miR-20b and up-regulation of miR-451a expression exhibits an anti-tumor effect in vitro (miR-20b: reduced viability, colony formation, increased apoptosis rate, and miR-451a: reduced colony forming ability). To summarize, the present study identified that expression of miR-20b and miR-451a are deregulated in vitro and in vivo and have a tumor suppressive role in GC through regulation of the PI3K/AKT/mTOR signaling pathway.

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Section: Discussionsupporting

confidence: 91%

miR-20b and miR-451a Are Involved in Gastric Carcinogenesis through the PI3K/AKT/mTOR Signaling Pathway: Data from Gastric Cancer Patients, Cell Lines and Ins-Gas Mouse Model

Streleckiene

Inčiūraitė

Juzėnas

et al. 2020

IJMS

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“…Among these 26 HCC-related RNA editing sites, the top three affected miRNAs were miR-17-3p, miR-20b-3p, and miR-593-3p (with 11, 7, and 7 target regulation changes induced by HCC-related editing sites, respectively ( Supplementary Table S5). Notably, miR-17-3p, miR-20b-3p, and miR-593-3p are widely involved in caner initiation and progression, including HCC (42)(43)(44)(45)(46). We observed that the expression levels of 163 RNA editing sites were correlated with the editing degree of corresponding genes, of which 10 were HCC-related editing sites.…”

Section: The Functional Consequence Of Rna Editing Sitesmentioning

confidence: 79%

Genomic Identification of RNA Editing Through Integrating Omics Datasets and the Clinical Relevance in Hepatocellular Carcinoma

Chen

Wang

et al. 2020

Front. Oncol.

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RNA editing is a widespread post-transcriptional mechanism to introduce single nucleotide changes to RNA in human cancers. Here, we characterized the global RNA editing profiles of 373 hepatocellular carcinoma (HCC) and 50 adjacent normal liver samples from The Cancer Genome Atlas (TCGA) and revealed that most editing events tend to occur in minor percentage of samples with moderate editing degrees (20-30%). Moreover, these RNA editing prefer to be A-to-I RNA editing in protein coding genes, especially in 3 ′ UTR regions. Considering the association between DNA mutation and RNA editing, our analysis found that RNA editing maybe a complementary event for DNA mutation of HCC risk genes in HCC patients. We next identified 454 HCC-related editing sites, and many locate on the same genes with the same editing patterns. The functional consequences of editing revealed 2,086 functional editing sites and demonstrated that most editing in coding regions are non-synonymous variations. Furthermore, our results showed that editing in the 3 ′ UTR regions tend to influence miRNA-target binding, and the editing degree seems to be negatively correlated with gene expression. Finally, we found that 46 HCC-related editing sites with consequence are able to distinguish the prognosis differences of HCC patients, suggesting their clinical relevance. Together, our results highlight RNA editing as a valuable molecular resource for investigating HCC mechanisms and clinical treatments.

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“…In addition, PTEN is regulated by miRNAs in ovarian, colon and breast cancer, glioma and other malignant tumors (28)(29)(30)(31). Notably, miR-20b regulates proliferation and migration of prostate cancer cells by directly targeting PTEN (12). Chu et al (32) demonstrated that the expression of PTEN is inhibited by miR-205, which is why miR-205 promotes proliferation and invasion of ovarian cancer cells.…”

Section: Discussionmentioning

confidence: 99%

“…miR-20b belongs to the miR-106a-363 gene cluster, and together with the miR-17-92 and miR-106b-25 clusters, it forms the miR-17 gene (9), which is active in the oncogenesis of certain types of human tumor (10). Increased miR-20b expression has previously been associated with decreased survival rate in gastric cancer (11), promotion of proliferation and migration of prostate cancer cells (12), and proliferation and DNA synthesis of breast cancer cells (13). miR-20b expression is altered in hepatocellular carcinoma, although its activity has not yet been described.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑20b promotes proliferation of H22 hepatocellular carcinoma cells by targeting PTEN

Luo

et al. 2019

Oncol Lett

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MicroRNAs (miRNAs/miRs) are small, noncoding RNA molecules that are closely associated with the occurrence and development of tumors. miR-20b is overexpressed in hepatocellular carcinoma cell lines and tissues. However, it is not clear whether miR-20b can promote the proliferation of hepatocellular carcinoma cells. In the present study, the proliferation of H22 mouse hepatocellular carcinoma cells was detected using the Cell Counting Kit-8 assay. MiRanda software was used to predict the binding sites of miR-20b to the 3'-untranslated region (3'-UTR) of phosphatase and tensin homolog (PTEN). The 3'-UTR sequence of the PTEN gene was amplified using the polymerase chain reaction in H22 cells. The recombinant plasmid or empty plasmid was co-transfected with miR-20b mimics or miR-20b scramble into HeLa cells, and luciferase activity was assessed by Dual-Luciferase ® Reporter Assay System 24 h post-transfection. In the present study, miR-20b knockdown significantly inhibited the proliferation of H22 mouse hepatocellular carcinoma cells. In addition, miR-20b inhibition upregulated the expression of PTEN, and it was revealed that miR-20b may directly target the 3'-untranslated region of the PTEN gene. Downregulation of PTEN partially reversed the anti-proliferative effect of miR-20b on H22 cells. In conclusion, miR-20b may promote H22 cell proliferation by targeting PTEN, providing a rationale for further study investigating novel therapeutic strategies for liver cancer.

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miR‑20b promotes cellular proliferation and migration by directly regulating phosphatase and tensin homolog in prostate cancer

Cited by 24 publications

References 38 publications

miR-20b and miR-451a Are Involved in Gastric Carcinogenesis through the PI3K/AKT/mTOR Signaling Pathway: Data from Gastric Cancer Patients, Cell Lines and Ins-Gas Mouse Model

miR-20b and miR-451a Are Involved in Gastric Carcinogenesis through the PI3K/AKT/mTOR Signaling Pathway: Data from Gastric Cancer Patients, Cell Lines and Ins-Gas Mouse Model

Genomic Identification of RNA Editing Through Integrating Omics Datasets and the Clinical Relevance in Hepatocellular Carcinoma

MicroRNA‑20b promotes proliferation of H22 hepatocellular carcinoma cells by targeting PTEN

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