miR-106a* inhibits the proliferation of renal carcinoma cells by targeting IRS-2

Ma, Yadong; Zhang, Hongyi; He, Xijing; Song, Haoming; Qiang, Yayong; Li, Yang; Gao, Jixue; Wang, Ziming

doi:10.1007/s13277-015-3605-x

Cited by 20 publications

(17 citation statements)

References 39 publications

(46 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…IRS2 is a member of the IRS family, which mainly interacts with SH2 domain-containing proteins to serve as adaptor proteins for additional surface receptors (37). IRS2 is overexpressed in several types of human cancer, including colorectal cancer (38), renal cell carcinoma (39), lung cancer (40) and breast cancer (41). It is a multifunctional oncogene that has been implicated in the regulation of numerous biological behaviors, such as cell proliferation, cell cycle, apoptosis, invasion and epithelial-mesenchymal transition (42)(43)(44).…”

Section: Discussionmentioning

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

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

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

View full text Add to dashboard Cite

show abstract

“…miR-106a inhibited glioma cell growth by targeting E2F1 independent of p53 status (25). miR-106a inhibited the proliferation of renal carcinoma cells by targeting IRS-2 (24). Moreover, miR-106a suppressed the proliferation, migration and invasion of osteosarcoma cells by targeting HMGA2 (22).…”

Section: Introductionmentioning

confidence: 99%

“…Upregulated expression of miR-106a by DNA hypomethylation played an oncogenic role in hepatocellular carcinoma by targeting TP53INP1 and CDKN1A (21). However, the expression of miR-106a was downregulated in glioma, renal carcinoma and osteosarcoma cancer (22)(23)(24). miR-106a inhibited glioma cell growth by targeting E2F1 independent of p53 status (25).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-106a promotes cell migration and invasion by targeting tissue inhibitor of matrix metalloproteinase 2 in cervical cancer

Zhou

Tao

et al. 2017

Oncology Reports

View full text Add to dashboard Cite

Abstract.Increasing evidence has demonstrated that miRNAs play a critical role in tumor development and progression. Previous studies have revealed that miR-106a is abnormally expressed in various cancers. However, its function and underlying mechanism in cervical cancer (CC) remains unknown. In this study, we confirmed that the expression of miR-106a was significantly upregulated in both CC cell lines and tissues by qRT-PCR. The increased expression of miR-106a was obviously associated with adverse prognostic features. Moreover, we demonstrated that miR-106a was a novel independent prognostic marker for predicting the 5-year survival of CC patients. The ectopic overexpression of miR-106a promoted cell migration, invasion and invasion-related gene expression, while downregulated miR-106a reversed the effect. In addition, miR-106a regulated tissue inhibitor of metalloproteinase (TIMP)2 by directly binding to its 3'-UTR, leading to the indution of the expression of matrix metalloproteinases (MMPs). In clinical samples of CC, miR-106a was inversely correlated with TIMP2, which was downregulated in CC. Alteration of TIMP2 expression at least partially abolished the migration, invasion and MMP expression of miR-106a in CC cells. In conclusion, our data indicated that miR-106a promoted the migration, invasion and MMP expression of CC by targeting TIMP2, and may represent a novel potential therapeutic target and prognostic marker for CC.

show abstract

“…Emerging evidence strongly suggests the critical roles of miRNAs in the pathogenesis of ovarian cancer, including miR-106a. To date, miR-106a has been found to be upregulated or downregulated in many types of cancers, such as renal carcinoma (5), colon cancer (6), esophageal carcinoma (7), gastric (8) and lung cancer (9). However, the mechanism of miR-106a in ovarian cancer is not clear, thus, we aimed to reveal the role of miR-106a in ovarian cancer.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-106a regulates phosphatase and tensin homologue expression and promotes the proliferation and invasion of ovarian cancer cells

et al. 2016

View full text Add to dashboard Cite

Abstract. Ovarian cancer is a leading cause of malignant gynecological tumor-related mortality among women. The treatment of ovarian cancer patients continues to be challenging. MicroRNA-106a (miR-106a) is widely expressed in diverse human tumors. In the present study, we investigated the biological and pathological roles of miR-106a in ovarian cancers. We found that miR-106a expression was significantly increased in primary ovarian cancer tissues and ovarian cancer cells compared with the level in normal tissues. Ectopic expression of an miR-106a inhibitor attenuated ovarian cancer cell proliferation and invasion. miR-106a promoted the growth and invasion of SKOV3 cells by targeting phosphatase and tensin homolog (PTEN). Furthermore, the present study revealed that IL-6 inhibited miR-106a expression by activating STAT3. Tocilizumab, a humanized anti-human IL-6R antibody, that competitively inhibits IL-6/IL-6R signaling, did not inhibit the proliferation and invasion of SKOV3 cells. In conclusion, our studies revealed that miR-106a was significantly increased in the ovarian cancer tissues and cell lines. Downregulation of the expression of miR-106a inhibited cell growth and metastasis of ovarian cancer cells. Together, the present study suggests that miR-106a acts as an oncogene in ovarian cancers.

show abstract

miR-106a* inhibits the proliferation of renal carcinoma cells by targeting IRS-2

Cited by 20 publications

References 39 publications

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

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

MicroRNA-106a promotes cell migration and invasion by targeting tissue inhibitor of matrix metalloproteinase 2 in cervical cancer

MicroRNA-106a regulates phosphatase and tensin homologue expression and promotes the proliferation and invasion of ovarian cancer cells

Contact Info

Product

Resources

About