MicroRNA-135b regulates the stability of PTEN and promotes glycolysis by targeting USP13 in human colorectal cancers

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Abstract

Dysregulation of microRNAs has been reported to be involved in the progression of human colorectal cancers (CRCs). Loss of the adenomatous polyposis coli (APC) gene is a common initiating event in CRCs. PTEN inactivation by mutation or allelic loss also occurs in CRCs. miR-135b was reported to be upregulated in CRCs and its overexpression was due to APC/β-catenin and PTEN/PI3K pathway deregulation. APC was proven to be a target of miR-135b and forms a feedback loop with miR-135b. In the present study, we found that ubiquitin-specific peptidase 13 (USP13) was a target of miR-135b. miR-135b downregulated the expression of USP13, and reduced the stability of PTEN. miR-135b promoted cell proliferation and glycolysis that could be reversed by the overexpression of USP13 or PTEN. Moreover, knockdown of USP13 upregulated the levels of endogenous miR-135b, but not those in CRC cells with PTEN mutation. The results showed positive feedback loops between miR-135b and PTEN inactivation in CRCs.

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Xiang, S., Fang, J., Wang, S., Deng, B., & Zhu, L. (2015). MicroRNA-135b regulates the stability of PTEN and promotes glycolysis by targeting USP13 in human colorectal cancers. Oncology Reports, 33(3), 1342–1348. https://doi.org/10.3892/or.2014.3694

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