CREB1, a direct target of miR-122, promotes cell proliferation and invasion in bladder cancer.

Oncology letters 2018

["Guo L", "Yin M", "Wang Y"]

Abstract

Bladder cancer (BC) is a prevalent cancer, which arises from the epithelial lining of the urinary bladder. CAMP-response element binding protein (CREB1) acts as a transcription factor, which regulates cell transcription through phosphorylation and dephosphorylation. The purpose of this study was to explore how miR-122 worked in BC on cell proliferation and invasion. RT-qPCR was applied to evaluate the mRNA levels of CREB1 and miR-122 in BC. CCK-8 and Transwell assays were employed to determine the migratory and invasive abilities. Dual luciferase reporter assay was applied to verify miR-122 targeting CREB1 in BC. CREB1 was upregulated in bladder tissues and T24, UM-UC-3 and J82 cells, while miR-122 upregulated and had negative correlation with CREB1. Moreover, knockdown of CREB1 inhibited cell proliferative and invasive capacities. In addition, CREB1 was directly targeted by miR-122 in BC and regulated its expression. We discovered that CREB1 could reverse partially the function of miR-122 on cell proliferation and invasion. CREB1 was mediated by miR-122, and regulated cell proliferation and invasiveness. The newly identified miR-122/CREB1 axis provides novel insight into the pathogenesis of BC.

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