Anti-miR-362-3p Inhibits Migration and Invasion of Human Gastric Cancer Cells by Its Target CD82

Yao, Yongliang; Wu, Xiaoyang; Wu, Jianhong; Gu, Tao; Chen, Ling; Gu, Jin-Hua; Liu, Yun; Xu, Ling

doi:10.1007/s10620-015-3563-6

Cited by 23 publications

(28 citation statements)

References 25 publications

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“…miR-362-3p has been shown to target oncogenes and exert beneficial effects. Expression of miR-362-3p has been investigated in several types of cancer and is negatively correlated with tumor progression in primary colorectal cancer (29)(30)(31)(32)(33)(34)(35)(36). MicroRNAs commonly target several genes.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA 362-3p Reduces hERG-related Current and Inhibits Breast Cancer Cells Proliferation

Assiri

Mourad

Shao

et al. 2019

Cancer Genomics Proteomics

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Background/Aim: hERG potassium channels enhance tumor invasiveness and breast cancer proliferation. MicroRNA (miRNA) dysregulation during cancer controls gene regulation. The objective of this study was to identify miRNAs that regulate hERG expression in breast cancer. Materials and Methods: Putative miRNAs targeting hERG were identified by bioinformatic approaches and screened using a 3'UTR luciferase assay. Functional assessments of endogenous hERG regulation were made using whole-cell electrophysiology, proliferation assays, and cell-cycle analyses following miRNA, hERG siRNA, or control transfection. Results: miR-362-3p targeted hERG 3'UTR and was associated with higher survival rates in patients with breast cancer (HR=0.39, 95%CI=0.18-0.82). Enhanced miR-362-3p expression reduced hERG expression, peak current, and cell proliferation in cultured breast cancer cells (p<0.05). Conclusion: miR-362-3p mediates the transcriptional regulation of hERG and is associated with survival in breast cancer. The potential for miR-362-3p to serve as a biomarker and inform therapeutic strategies warrants further investigation.

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Section: Discussionmentioning

confidence: 99%

MicroRNA 362-3p Reduces hERG-related Current and Inhibits Breast Cancer Cells Proliferation

Assiri

Mourad

Shao

et al. 2019

Cancer Genomics Proteomics

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“…Reportedly, CD82 overexpression significantly decreased the migratory and invasive abilities of gastric cancer cells with the hypoexpression of bFGF and uPA [9]. miR-362-3p expression induced the metastasis of gastric cancer cells by targeting CD82 with E-cadherin hypoexpression, N-cadherin, and vimentin hyperexpression [10]. In the present study, we performed a meta-and bioinformatics analysis to clarify the clinicopathological and prognostic significances of CD82 expression at both mRNA and protein levels.…”

Section: Introductionmentioning

confidence: 87%

The roles of CD82 expression in gastric cancer: a meta and bioinformatics analysis

Zheng¹,

Gong²

2017

Oncotarget

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CD82 encodes a transmembrane glycoprotein of tetraspanins family, and functions as a tumor metastasis suppressor. We performed a systematic meta and bioinformatics analysis through multiple online databases up to March 14, 2017. We¬ found down-regulated CD82 expression in gastric cancer, compared with normal mucosa (p < 0.05). CD82 expression was negatively with depth of invasion, lymph node and distant metastasis, TNM staging and dedifferentiation of gastric cancer (p < 0.05). A positive association between CD82 expression and favorable overall survival was found in patients with gastric cancer (p < 0.005). According to bioinformatics analysis, CD82 mRNA expression was higher in gastric cancer than normal tissues (p < 0.05). According to Kaplan-Meier plotter and TCGA database, we found that a higher CD82 expression was positively correlated with overall or progression-free survival rates of all cancer patients, even stratified by aggressive parameters or as an independent factor (p < 0.05). These findings indicated that CD82 expression might be employed as a potential marker to indicate gastric carcinogenesis and subsequent progression, even favorable prognosis.

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“…Real‐time PCR was carried out as described in our previous report . Total RNA was extracted using TRIzol Reagent (Invitrogen, San Diego, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

“…Western blot analysis was undertaken as described in our previous reports . Primary Abs were purchased from Abcam: for GAPDH (ab8235, diluted 1:3000) and CD82 (ab66400), Smad2/3 (ab63399), Smad4 (ab40759), E‐cadherin (ab76055), and N‐cadherin (ab98952; all diluted 1:1000).…”

Section: Methodsmentioning

confidence: 99%

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Interaction of transforming growth factor‐β‐Smads/microRNA‐362‐3p/CD82 mediated by M2 macrophages promotes the process of epithelial‐mesenchymal transition in hepatocellular carcinoma cells

et al. 2019

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Abnormal tumor microenvironment and the epithelial‐mesenchymal transition (EMT) are important features of tumor metastasis. However, it remains unknown how signals can form complicated networks to regulate the sustainability of the EMT process. The aim of our study is to explore the possible interaction between tumor‐associated macrophages and tumor cells in the EMT process mediated by microRNA (miR)‐362‐3p. In this study, we found that by releasing TGF‐β, M2 macrophages mediate binding of Smad2/3 to miR‐362‐3p promoter, leading to overexpression of miR‐362‐3p. MicroRNA‐362‐3p maintains EMT by regulating CD82, one of the most important members of the family of tetraspanins. Our finding suggests that miR‐362‐3p can serve as a core factor mediating cross‐talk between the TGF‐β pathway in tumor‐associated macrophages and tetraspanins in tumor cells, and thus facilitates the EMT process.

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Anti-miR-362-3p Inhibits Migration and Invasion of Human Gastric Cancer Cells by Its Target CD82

Abstract: This study illuminated that downregulation of miR-362-3p along with the upregulation of CD82 in GC cells resulted in the inhibition of GC migration and invasion. Thus, our results suggested that miR-362-3p or CD82 can be exploited as a new potential target for control of GC in the future.

Cited by 23 publications

References 25 publications

MicroRNA 362-3p Reduces hERG-related Current and Inhibits Breast Cancer Cells Proliferation

MicroRNA 362-3p Reduces hERG-related Current and Inhibits Breast Cancer Cells Proliferation

The roles of CD82 expression in gastric cancer: a meta and bioinformatics analysis

Interaction of transforming growth factor‐β‐Smads/microRNA‐362‐3p/CD82 mediated by M2 macrophages promotes the process of epithelial‐mesenchymal transition in hepatocellular carcinoma cells

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