MicroRNA‐218 inhibits tumor growth and increases chemosensitivity to CDDP treatment by targeting BCAT1 in prostate cancer

Zhu, Wenjing; Shao, Yiye; Peng, Yu

doi:10.1002/mc.22612

Cited by 32 publications

(23 citation statements)

References 32 publications

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“…Notably, Xu et al have demonstrated that overexpression of BCAT1 indicates a poor survival of GC and may serve as a diagnostic and therapeutic biomarker [19]. BCAT1 usually exerts its function in regulating the tumorigenesis as a downstream target of miRNAs [34,35]. In this study, BCAT1 was determined to be a target of miR-3200-5p, which was negatively regulated by miR-3200-5p.…”

Section: Discussionmentioning

confidence: 67%

Silencing of Long Noncoding RNA LINC00324 Interacts with MicroRNA-3200-5p to Attenuate the Tumorigenesis of Gastric Cancer via Regulating BCAT1

Wang

Cheng

Yang

et al. 2020

Gastroenterology Research and Practice

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Purpose. This study was aimed at exploring the effect of long noncoding RNA LINC00324 (LINC00324) on gastric cancer (GC) and the potential molecular mechanisms. Methods. The expression of LINC00324 and miR-3200-5p in GC tissues and cells was detected by qRT-PCR. LINC00324 was silenced in GC cells by transfection of si-LINC00324. Then, the proliferation, migration, and invasion of GC cells were analyzed by MTT, wound healing, and transwell assays, respectively. The interactions between LINC00324 and miR-3200-5p and between miR-3200-5p and BCAT1 were determined by a dual-luciferase reporter and/or RNA pull-down assay. Results. The expression of LINC00324 was upregulated in GC cells and tissues, but miR-3200-5p was downregulated. Silencing of LINC00324 inhibited the proliferation, migration, and invasion of GC cells. LINC00324 directly targeted miR-3200-5p, and miR-3200-5p directly targeted BCAT1. si-LINC00324 negatively regulated BCAT1 expression via binding to miR-3200-5p. Furthermore, silencing of LINC00324 reversed the promoting effects of BCAT1 on the proliferation, migration, and invasion of GC cells. Conclusion. Silencing of LINC00324 inhibited the proliferation, migration, and invasion of GC cells through regulating the miR-3200-5p/BCAT1 axis.

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Section: Discussionmentioning

confidence: 67%

Silencing of Long Noncoding RNA LINC00324 Interacts with MicroRNA-3200-5p to Attenuate the Tumorigenesis of Gastric Cancer via Regulating BCAT1

Wang

Cheng

Yang

et al. 2020

Gastroenterology Research and Practice

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“… 29 miR-218 inhibited tumor growth and increased chemosensitivity to cisplatin in prostate cancer via negatively regulating BCAT1 protein expression. 30 In glioma cells, miR-218 affected cell proliferation, apoptosis, and invasion by negatively modulating HMGB-mediated suppression of receptor for advanced glycation end products. 31…”

Section: Discussionmentioning

confidence: 99%

<em>miR-218</em> overexpression suppresses tumorigenesis of papillary thyroid cancer via inactivation of PTEN /PI3K/AKT pathway by targeting Runx2

Han¹,

Chen²,

Wang³

2018

OTT

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BackgroundIt was previously reported that downregulation of miR-218 promoted thyroid cancer cell invasion, migration, and proliferation. However, the biological functions of miR-218 and its possible regulatory mechanisms in papillary thyroid cancer (PTC) cells are still elusive.Materials and methodsThe expression levels of miR-218 and Runx2 in PTC tissues and cells were determined by quantitative real-time PCR (qRT-PCR) and Western blot. The effects of miR-218 overexpression on cell viability, invasion, apoptosis, and PTEN/PI3K/AKT pathway in PTC cells were evaluated by cell counting kit-8 assay, Transwell invasion assay, flow cytometry assay, and Western blot, respectively. Luciferase reporter assay and qRT-PCR were performed to identify the target of miR-218. Xenograft tumor experiment was performed to confirm the biological roles of miR-218 and its potential mechanisms in vivo.ResultsmiR-218 expression was downregulated and Runx2 expression was upregulated in PTC tissues and cells. Overexpression of miR-218 suppressed viability and invasion, and induced apoptosis of PTC cells in vitro, while Runx2 overexpression greatly abolished these effects. miR-218 overexpression inactivated the PTEN/PI3K/AKT pathway, which was abated by Runx2 upregulation. Additionally, Runx2 was validated to be a direct target of miR-218. Moreover, enforced expression of miR-218 inhibited tumor growth and Runx2 expression, and blocked PTEN/PI3K/AKT pathway in vivo.ConclusionmiR-218 overexpression suppresses the tumorigenesis of PTC via downregulating PTEN/PI3K/AKT pathway by targeting Runx2, which indicates that miR-218 may be a potential therapeutic target for human PTC.

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“…MiR-218 involves in inhibition of GC cell growth and invasion through targeting Angiopoietin-2 [ 27 ]. Additionally, in prostate cancer, miR-218 acts as a suppressor for tumor cell proliferation [ 28 ]. For HCC, miR-218 has been validated as a down-regulated genes associated with tumor process through targeting different downstream mRNAs, such as PTEN, E2F2 [ 29 , 30 ].…”

Section: Discussionmentioning

confidence: 99%

Integrative bioinformatics analysis identifies ROBO1 as a potential therapeutic target modified by miR-218 in hepatocellular carcinoma

et al. 2017

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Patients diagnosed with advanced hepatocellular carcinoma (HCC) presented poor prognosis and short survival time. Althouth accumulating contribution of continuous research has gradually revealed complex tumorigenesis mechanism of HCC with numerous and jumbled biomarkers, those specific ones for HCC diagnose and therapeutic treatment are required illustration. Multiple genes over-expressed in HCC specimens with at least 1.5 fold change were cohorted, compared with the non-cancerous tissues through integrative bioinformatics analysis from Gene Expression Omnibus (GEO) datasets GSE14520 and GSE6764, including 445 and 45 cases of samples spearatly, along with intensive exploration on the Cancer Genome Altas (TCGA) dataset of liver cancer. Thirteen genes significantly highly expressed, overlapping in the datasets above. The Database for Annotation Visualization and Integrated Discovery (DAVID) program was utilized for functional pathway enrichment analysis. Protein-protein Interaction (PPI) analysis was conducted through the Search Tool for the Retrieval of Interacting Genes (STRING) database. ROBO1 was highlighted as one of the most probable molecules among the 13 candidates participating in cancer process. Cancer Cell Line Encycolopedia (CCLE) database was utilized exploring ROBO1 expression in cell lines. Immunochemistry analysis and qRT-PCR assay were performed in our medical center, which indicates significant over-expression status in either HCC tumor specimens and 3 HCC cell lines. Furtherly, we recognized that miR-218, a tumor suppressor, might be an upstream regulator for ROBO1 directly binding to the mRNA 3’UTR and potentially modifying the expression and function of ROBO1. Herein, we conclude that ROBO1 is a mighty therapeutic targets modified by miR-218 in HCC deserving further investigation.

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MicroRNA‐218 inhibits tumor growth and increases chemosensitivity to CDDP treatment by targeting BCAT1 in prostate cancer

Cited by 32 publications

References 32 publications

Silencing of Long Noncoding RNA LINC00324 Interacts with MicroRNA-3200-5p to Attenuate the Tumorigenesis of Gastric Cancer via Regulating BCAT1

Silencing of Long Noncoding RNA LINC00324 Interacts with MicroRNA-3200-5p to Attenuate the Tumorigenesis of Gastric Cancer via Regulating BCAT1

<em>miR-218</em> overexpression suppresses tumorigenesis of papillary thyroid cancer via inactivation of PTEN /PI3K/AKT pathway by targeting Runx2

Integrative bioinformatics analysis identifies ROBO1 as a potential therapeutic target modified by miR-218 in hepatocellular carcinoma

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