DNA‐methylation‐mediated repression of miR‐766‐3p promotes cell proliferation via targeting SF2 expression in renal cell carcinoma

Chen, Chen; Xue, Sheng; Zhang, Jin; Chen, Wei; Gong, Dongkui; Zheng, Jiayi; Ma, Junjie; Xue, Wei; Chen, Yonghui; Zhai, Wei; Zheng, Junhua

doi:10.1002/ijc.30853

Cited by 54 publications

(53 citation statements)

References 44 publications

(79 reference statements)

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“…For instance, miR-766 was reported to promote cell proliferation in colorectal cancer by targeting SOX6 expression (12). In renal cell carcinoma, miR-766 overexpression attenuated cell-cycle progression by down-regulating SF2 expression (21). In this study, our results showed that miR-766 was up-regulated in HCC tissues and that up-regulation of miR-766 promotes the proliferation and metastasis of HCC cells by directly decreasing the NR3C2 expression.…”

Section: Discussionsupporting

confidence: 53%

MicroRNA‐766 promotes cancer progression by targeting NR3C2 in hepatocellular carcinoma

Yang

Guan

et al. 2018

The FASEB Journal

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MicroRNAs (miRNAs) have been reported to play important roles in tumor progression of various cancers. However, the clinical significance and biologic function of miR-766 in hepatocellular carcinoma (HCC) remain unknown. In this study, we investigated the roles of miR-766 in HCC progression using HCC cell lines and a xenograft mouse model. miR-766 expression in tumor tissues and adjacent nontumorous liver tissues of patients with HCC was evaluated by quantitative RT-PCR. Our results showed that miR-766 promoted proliferation and metastasis of HCC cells in vitro and in vivo and that NR3C2 was a direct target of miR-766 and involved in miR-766-mediated proliferation and metastasis of HCC cells. We also found that miR-766 affected the β-catenin signaling pathway by targeting NR3C2. Furthermore, miR-766 was significantly up-regulated in HCC tissues and was correlated with the prognosis of patients with liver cancer. Taken together, our results show that miR-766 affects HCC progression by modulating NR3C2 expression and is a possible new therapeutic target for patients with HCC.-Yang, C., Ma, X., Guan, G., Liu, H., Yang, Y., Niu, Q., Wu, Z., Jiang, Y., Bian, C., Zang, Y., Zhuang, L. MicroRNA-766 promotes cancer progression by targeting NR3C2 in hepatocellular carcinoma.

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Section: Discussionsupporting

confidence: 53%

MicroRNA‐766 promotes cancer progression by targeting NR3C2 in hepatocellular carcinoma

Yang

Guan

et al. 2018

The FASEB Journal

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“…Expression of miR-766 is decreased in renal cell carcinoma, and low miR-766 expression is significantly correlated with the clinical stage. In addition, patients with renal cell carcinoma and low miR-766 expression exhibit poorer prognosis compared with those patients with high miR-766 expression (23). Conversely, miR-766 is overexpressed in lung adenocarcinoma (24) and colorectal cancer (25).…”

Section: Discussionmentioning

confidence: 99%

“…miR-766 has been well studied in numerous types of human cancer, including renal cell carcinoma (23), lung adenocarcinoma (24) and colorectal cancer (25). However, the expression status, specific roles and regulatory mechanisms of miR-766 in PTC remain largely unclear.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑766 inhibits papillary thyroid cancer progression by directly targeting insulin receptor substrate 2 and regulating the PI3K/Akt pathway

Zhao

Chen

et al. 2018

Int J Oncol

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MicroRNAs (miRNAs/miRs) are widely dysregulated in papillary thyroid cancer (PTC). Dysregulated miRNAs, together with their target genes, comprise a complex network that has been implicated in the regulation of PTC pathogenesis. Further knowledge of the functional roles of aberrantly expressed miRNAs in PTC, and the underlying molecular mechanisms, may assist in the identification of novel therapeutic targets. miR-766 has been well studied in human cancer; however, the expression status, specific roles and regulatory mechanisms of miR-766 in PTC remain unclear. The present study aimed to detect miR-766 expression in PTC tissues and cell lines, to explore the biological roles of miR-766 in the malignant biological behaviors of PTC cells, and to determine the underlying mechanism of action of miR-766 in PTC cells. The results revealed that miR-766 was downregulated in PTC tissues and cell lines, and its downregulation was strongly associated with TNM stage and lymph node metastasis. Overexpression of miR-766 inhibited PTC cell proliferation, colony formation, migration and invasion, promoted cell apoptosis and reduced tumor growth in vivo. Mechanistically, insulin receptor substrate 2 (IRS2) was identified as a direct target of miR-766 in PTC cells. IRS2 was upregulated in PTC tissues, and this was inversely correlated with miR-766 expression. Inhibition of IRS2 simulated the tumor suppressor activity of miR-766 in PTC cells. Restoration of IRS2 expression negated the tumor-suppressing effects of miR-766 overexpression on PTC cells. Notably, miR-766 directly targeted IRS2 to inhibit activation of the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) pathway in PTC cells in vitro and in vivo. Overall, these findings indicated that miR-766 may inhibit the malignant biological behaviors of PTC cells by directly targeting IRS2 and regulating the PI3K/Akt pathway, thus suggesting that this miRNA may be a promising therapeutic target for PTC.

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“…Renal cell carcinoma (RCC) is one of the most aggressive human urological malignancies, accounting for 2%-3% of adult malignancies [15; 39]. One third of patients have metastatic lesions detected at primary diagnosis, and 30% eventually develop metastatic renal cell carcinoma (mRCC) after surgery [2]. Because of its resistance to radiotherapy and chemo-therapy, surgical resection remains the unique effective treatment [1; 25].…”

Section: Introductionmentioning

confidence: 99%

Preclinical Study: Sunitinib-suppressed MiR-452-5p Facilitates Renal Cancer Cell Invasion and Metastasis Through Modulating SMAD4/SMAD7/EMT Signals

Zhai

Zhang

et al. 2018

Preprint

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Although microRNAs (miRNAs) have been revealed as crucial modulators in tumor metastasis and target therapy, our understanding of their roles in metastatic renal cell carcinoma (mRCC) and Sunitinib treatment is limited. Here, We focused on 2 published microarray data to select out our anchored miRNA which was downregulated after Sunitinib treatment while upregulated in metastasis RCC tissues.Then we discovered that treating with Sunitinib, the targeted receptor tyrosine kinase inhibitor (TKI), inhibited renal cell migration and invasion via attenuating the expression of miR-452-5p. The novel identified miR-452-5p was upregulated and associated with poor prognosis in RCC. Preclinical studies using multiple RCC cells and xenografts model illustrated that miR-452-5p could promote RCC cell migration and invasion in vitro and in vivo. Mechanistically, P65 could directly bind to the miR-452-5p promoter and thus transcriptionally induce miR-452-5p expression, which led to post-transcriptionally abrogate SMAD4 expression, thus inhibition of its downstream signals including SMAD7 and EMT (Epithelial-Mesenchymal Transition) associated genes. Our study presented a road map for targeting this newly identified miR-452-5p and its SMAD4/SMAD7/EMT signals pathway, which imparted a new potential therapeutic strategy for mRCC treatment.

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DNA‐methylation‐mediated repression of miR‐766‐3p promotes cell proliferation via targeting SF2 expression in renal cell carcinoma

Cited by 54 publications

References 44 publications

MicroRNA‐766 promotes cancer progression by targeting NR3C2 in hepatocellular carcinoma

MicroRNA‐766 promotes cancer progression by targeting NR3C2 in hepatocellular carcinoma

MicroRNA‑766 inhibits papillary thyroid cancer progression by directly targeting insulin receptor substrate 2 and regulating the PI3K/Akt pathway

Preclinical Study: Sunitinib-suppressed MiR-452-5p Facilitates Renal Cancer Cell Invasion and Metastasis Through Modulating SMAD4/SMAD7/EMT Signals

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