Upregulation of microRNA-370 promotes cell apoptosis and inhibits proliferation by targeting PTEN in human gastric cancer

Yang, Zunhua; Fu, Meng; Wu, Gang-Wei; Zhang, An-Zu; Chen, Jinping; Lin, Hong-Yue; Fu, Yongan; Jia, Jing; Cai, Zhengdong; Wu, Xiaojian; Lan, Ping

doi:10.3892/ijo.2016.3642

Cited by 22 publications

(12 citation statements)

References 38 publications

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“…Our research found that miR-370 was also downregulated in GC and could function as a tumor suppressor via targeting EGFR. This is consistent with the result from one previous study in which upregulation of miR-370 promoted cell apoptosis and inhibited proliferation via targeting PTEN in human GC (21). However, studies also found that upregulation of miR-370 contributed to the progression of gastric carcinoma (36,37).…”

Section: Discussionsupporting

confidence: 92%

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miR-370 regulates cell proliferation and migration by targeting EGFR in gastric cancer

et al. 2017

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Epidermal growth factor receptor (EGFR) is known to be overexpressed in ~30% of gastric cancer (GC) cases, and may serve as an effective biomarker for predicting the clinical benefit of anti-EGFR therapy. However, the mechanism underlying the regulation of EGFR expression remains unknown. Evidence indicates that post-transcriptional regulation may exist in the process of EGFR expression. In the present study, we aimed to explore whether miR-370 is involved in this process, and how it impacts the biological behaviors of GC cells. In the present study, we first determined the role of EGFR in GC by means of an EGFR overexpression plasmid and siRNAs. Then, the expression levels of EGFR protein and mRNA in GC tissues were analyzed through immunohistochemistry and quantitative RT-PCR (RT-qPCR). Bioinformatics tools and dual-luciferase assay were applied to predict and validate the relevant miRNA targeting EGFR. Finally, human GC MGC-803 cells were selected to explore the effect of miRNA on cell proliferation and migration. We found that suppression of EGFR inhibited the proliferation and migration of GC cells. In addition, the levels of EGFR protein in the GC tissues were ~4 times higher than that in the corresponding paired non-cancerous tissues while the mRNA levels of EGFR were only ~2-fold as high as that in the adjacent non-cancerous tissues. Bioinformatics tools predicted that miRNA-370 was a regulator of EGFR and dual‑luciferase assay validated that miR-370 could directly bind to the 3'-untranslated region (3'-UTR) of EGFR mRNA. Meanwhile, an inverse correlation between miR-370 and EGFR was found in the GC tissues. Overexpression of miR-370 suppressed the proliferation and migration of GC cells, while downregulation of miR-370 promoted proliferation and migration. The present study may provide new information for understanding the molecular mechanism underlying the regulation of EGFR protein expression in GC and may be of important clinical significance to guide targeted therapy.

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Section: Discussionsupporting

confidence: 92%

“…In a previous study, miR-370 was reported to function as a tumor suppressor in colorectal cancer by suppressing EGFR signaling (20). It has been reported that miR-370 is also significantly downregulated in GC (21). However, whether EGFR protein expression is regulated by miR-370 in GC remains unknown.…”

Section: Introductionmentioning

confidence: 99%

miR-370 regulates cell proliferation and migration by targeting EGFR in gastric cancer

et al. 2017

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“…Biological functions for PTEN have been demonstrated in mediating several cell processes, including cell growth, adhesion, metastasis and apoptosis [29,30]. Further, PTEN has been clarified as a direct target of various miRNAs, such as miR-19b, miR-93 and miR-370 [31][32][33]. In the current study, we appraised PTEN expression in H9c2 cells with Orid and hypoxia co-management or miR-214 inhibitor transfection.…”

Section: Discussionmentioning

confidence: 96%

Oridonin relieves hypoxia-evoked apoptosis and autophagy via modulating microRNA-214 in H9c2 cells

Gong

Zhang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Oridonin (Orid) has been diffusely applied to remedy dissimilar cancers. Howbeit, the influence of Orid in ischemic heart disease (IHD) remains imprecise. The current study uncovered the functions of Orid in hypoxia-caused apoptosis and autophagy in H9c2 cells. H9c2 cells received hypoxia and Orid manipulation, cell viability, apoptosis, apoptosis-interrelated factors and autophagy-correlative factors were appraised. After the extraordinary vectors transfections, the impacts of miR-214 inhibition on hypoxia-triggered apoptosis and autophagy were investigated. Further, dual luciferase reporter assay was enforced for ascertaining the pertinence between miR-214 and PTEN. PI3K/AKT/mTOR pathway was finally determined using western blot. We found that, Orid significantly alleviated hypoxia-induced apoptosis and autophagy through regulation their associated proteins in H9c2 cells. Up-regulation of miR-214 was found in hypoxia and Orid co-managed cells, meanwhile, repression of miR-214 obviously annulled the modulatory functions of Orid in hypoxia-evoked apoptosis and autophagy. Additionally, PTEN was forecasted to be a firsthand target of miR-214. Besides, we observed that Orid evoked PI3K/ AKT/mTOR activation through elevation of miR-214 in hypoxia-managed H9c2 cells. In conclusion, the amusing results corroborated that Orid relieved hypoxia-caused apoptosis and autophagy via adjusting PI3K/AKT/mTOR pathway through enhancement of miR-214 in H9c2 cells.

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“…Recently, case series studies demonstrated the expression and function of miR-370 in cancer. Previous studies showed that miR-370 is decreased in the tissues and cell lines of gastric cancer and overexpression of miR-370 promotes cell apoptosis and inhibits proliferation ( 15 , 16 ). In non-small cell lung cancer tissues and cell lines, miR-370 expression was also downregulated, and upregulation of miR-370 impaired tumor growth by inhibiting cell proliferation ( 17 ).…”

Section: Discussionmentioning

confidence: 99%

MiR‑370 promotes apoptosis in colon cancer by directly targeting MDM4

et al. 2017

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MicroRNA (miR)-370 functions as a tumor suppressor or promoter in several cancers. However, the expression and biological role of miR-370 in colon cancer remains undefined. In the present study, miR-370 expression in both normal and malignant colon tissues was quantified by quantitative polymerase chain reaction. An in vitro cell viability and apoptosis assay and an in vitro xenograft tumor model were employed to investigate the role of miR-370 on colon cancer growth. Furthermore, the potential direct target of miR-370 was identified using a luciferase assay. Our results demonstrate that down-regulation of miR-370 expression occurs in malignant tissues and miR-370 expression is inversely correlated with tumor grade. Moreover, we determined that miR-370 functions as a tumor suppressor in colon cancer by inhibiting cell proliferation and promoting cell apoptosis. In addition, overexpression of miR-370 impairs xenograft tumor growth in nude mice. Mechanistically, mouse double minute 4 (MDM4) was demonstrated to be a potential direct target of miR-370, inducing apoptosis in colon cancer. Collectively, these findings suggest that upregulation of miR-370 may impair colon tumor growth by directly targeting MDM4. These findings provide a new direction for the diagnosis and treatment of colon cancer.

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Upregulation of microRNA-370 promotes cell apoptosis and inhibits proliferation by targeting PTEN in human gastric cancer

Cited by 22 publications

References 38 publications

miR-370 regulates cell proliferation and migration by targeting EGFR in gastric cancer

miR-370 regulates cell proliferation and migration by targeting EGFR in gastric cancer

Oridonin relieves hypoxia-evoked apoptosis and autophagy via modulating microRNA-214 in H9c2 cells

MiR‑370 promotes apoptosis in colon cancer by directly targeting MDM4

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