MiR-17-5p regulates cell proliferation and migration by targeting transforming growth factor-β receptor 2 in gastric cancer

Qu, Yanjun; Zhang, Haiyang; Duan, Jingjing; Li, Rui; Deng, Ting; Bai, Ming; Huang, Dingzhi; Liu, Hongli; Ning, Tao; Zhang, Le; Wang, Xia; Ge, Shaohua; Zhou, Lyu; Zhong, Benfu; Ying, Guoguang; Ba, Yi

doi:10.18632/oncotarget.8946

Cited by 42 publications

(36 citation statements)

References 37 publications

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“…In addition, forced expression of miR-491-5p inhibited tumor proliferation, disrupted the cell cycle, and induced apoptosis in vitro and in vivo [49]. We also showed that lncRNA RP11-363E7.4 interacted with three miRNAs (miR-17-5p, miR-19b-3p, and miR-106a-5p), which were previously investigated in the reports of Xia et al, Zhang et al, and Qu et al [22,50,51]. …”

Section: Random Walk With Restart Analyses Of a Gc-related Lncrna-mrnsupporting

confidence: 65%

A Novel LncRNA-miRNA-mRNA Triple Network Identifies LncRNA RP11-363E7.4 as An Important Regulator of miRNA and Gene Expression in Gastric Cancer

Wang

Zhao

et al. 2018

Cell Physiol Biochem

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Background/Aims: Recent evidence has shown that some long non-coding RNAs (lncRNAs) play important roles in various biological processes. However, the regulatory mechanism of lncRNA in gastric cancer (GC) remains unclear. Methods: We reannotated the GC gene expression profile into a lncRNA-mRNA biphasic profile and integrated the microRNA target data to construct a global GC triple network. A further clustering and random walk with restart analyses was performed on the triple network from the level of topology analyses. Quantitative real-time PCR was used to determine expression of lncRNA RP11-363E7.4. Kaplan-Meier analyses was performed to evaluate the prognostic value of lncRNA RP11-363E7.4. Results: We constructed a gastric cancer lncRNA-miRNA-mRNA network (GCLMN) including six lncRNAs, 332 mRNAs, and 3,707 edges. For the shared lncRNA RP11-363E7.4, the interacting gene and microRNA functional enrichment studies implied that lncRNA RP11-363E7.4 might function as a new regulator in GC. The expression of lncRNA RP11-363E7.4 was downregulated compared with that of paracarcinoma tissues in five GC samples. High expression of lncRNA RP11-363E7.4 was found to be correlated to better overall survival (OS) for GC patients. Conclusions: This study focused on GC lncRNA-miRNA-mRNA regulatory networks, and found that lncRNA RP11-363E7.4 was a new GC risk lncRNA, which might provide novel insight into a better understanding of the pathogenesis of GC.

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Section: Random Walk With Restart Analyses Of a Gc-related Lncrna-mrnsupporting

confidence: 65%

A Novel LncRNA-miRNA-mRNA Triple Network Identifies LncRNA RP11-363E7.4 as An Important Regulator of miRNA and Gene Expression in Gastric Cancer

Wang

Zhao

et al. 2018

Cell Physiol Biochem

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“…Because of the stability of miRNA, many studies regard it as a biomarker in human cancers, by acting as oncogenes or suppressors [23,24]. In various types of cancers, miRNA-related pathways is a heat-point, such as miR-17 and miR-29a/c in gastric cancer [25,26], miR-135b in colorectal cancer [27], miR-106a in cholangiocarcinoma [28]. MiRNAs are also related to development and progression of GC [29].…”

Section: Effects Of Egfr On Proliferation and Migration In Gc Cellsmentioning

confidence: 99%

MiR-520b/e Regulates Proliferation and Migration by Simultaneously Targeting EGFR in Gastric Cancer

Zhang

Ning

et al. 2016

Cell Physiol Biochem

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Background: MicroRNAs (miRNAs) have been demonstrated to play a crucial role in tumorigenesis. Previous studies have shown that miR-520b/e acts as a tumor suppressor in several tumors. Other studies indicated that epidermal growth factor receptor (EGFR) is highly expressed in many tumors, and involved in the development of tumors, such as cell proliferation, migration, angiogenesis and apoptosis. However, the correlation of miRNAs and EGFR in gastric cancer (GC) has not been adequately investigated. Our aim was to explore the relationship. Methods: The expression levels of EGFR and miR-520b/e were examined by RT-PCR and Western blot. We also investigated the relationship between EGFR and miR-520b/e in GC cell lines by relevant experiments. Results: In this study, we found that miR-520b/e inhibits the protein expression of EGFR by directly binding with the 3'-untranslated region (3'-UTR). And it was shown that the down-regulation of miR-520b/e promotes cell proliferation and migration by negative regulation of the EGFR pathway, while over-expression of miR-520b/e inhibits these properties. In addition, the biological function of EGFR in GC cell lines was validated by silencing and over-expression assays respectively. Conclusions: Taken together, our results demonstrate that miR-520b/e acts as a tumor suppressor by regulating EGFR in GC, and provide a novel marker and insight for the potential therapeutic target of GC.

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“…Previous studies have demonstrated that expression levels of miRNAs are associated with cancer initiation and progression (15)(16)(17). The abnormal expression of miRNAs may suggest oncogenic or tumor suppressive functions of miRNAs in cancer, dependent on the tumor type and the target genes of the miRNA (18). Therefore, further studies on the regulatory mechanisms of miRNAs in cancer may provide an improved understanding of the oncogenes is network and potential therapeutic targets for cancer treatment.…”

Section: Introductionmentioning

confidence: 99%

Microrna-136 promotes proliferation and invasion ingastric cancer cells through Pten/Akt/P-Akt signaling pathway

2018

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Abstract. Gastric cancer is the fourth most common cancer and the second most frequent cause of cancer-associated mortality in the world. Previous studies have revealed that expression levels of microRNAs (miRNAs) are associated with the initiation and progression of several types of cancer, including gastric cancer. Previous studies have demonstrated that the abnormal expression of miRNA-136 may serve a function in the progression of several types of human cancer. However, the expression pattern of miR-136, its functions and underlying molecular mechanisms in gastric cancer remain unresolved. In the present study, it was revealed that the expression of miR-136 was aberrantly up regulated in gastric cancer tissues and cell lines. The suppression of miR-136 was able to inhibit proliferation and invasion in gastric cancer cell lines. Furthermore, phosphatase and tensin homolog (PTEN) was identified as a direct target gene of miR-136 in gastric cancer. PTEN was under expressed in gastric cancer tissues compared with non-tumor gastric tissues, and PTEN expression was negatively correlated with miR-136 expression. Furthermore, PTEN overexpression mimics the effects of miR-136 knockdown on gastric cancer cells. Additionally, miR-136 under expression decreased phospho-(p) AKT expression, but did not affect AKT expression in gastric cancer cells. In conclusion, the data of the present study suggest that miR-136 acts as an oncogene in gastric cancer via regulation of the PTEN/AKT/p-AKT signaling pathway and may potentially serve as a novel therapeutic target for the treatment of gastric cancer.

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MiR-17-5p regulates cell proliferation and migration by targeting transforming growth factor-β receptor 2 in gastric cancer

Cited by 42 publications

References 37 publications

A Novel LncRNA-miRNA-mRNA Triple Network Identifies LncRNA RP11-363E7.4 as An Important Regulator of miRNA and Gene Expression in Gastric Cancer

A Novel LncRNA-miRNA-mRNA Triple Network Identifies LncRNA RP11-363E7.4 as An Important Regulator of miRNA and Gene Expression in Gastric Cancer

MiR-520b/e Regulates Proliferation and Migration by Simultaneously Targeting EGFR in Gastric Cancer

Microrna-136 promotes proliferation and invasion ingastric cancer cells through Pten/Akt/P-Akt signaling pathway

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