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miR-130b promotes bladder cancer cell proliferation, migration and invasion by targeting VGLL4
Author(s) -
Xiaowu Liu,
Chuize Kong,
Zhe Zhang
Publication year - 2018
Publication title -
oncology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.094
H-Index - 96
eISSN - 1791-2431
pISSN - 1021-335X
DOI - 10.3892/or.2018.6300
Subject(s) - cell growth , oncogene , reporter gene , transfection , microrna , cell cycle , gentamicin protection assay , cell , cell migration , biology , cancer research , microbiology and biotechnology , cell culture , viability assay , bladder cancer , mtt assay , cancer , gene expression , metastasis , gene , genetics
Bladder cancer (BCa) is the most common urological cancer, and more and more evidence suggests that microRNAs (miRNAs) play an important role in BCa pathogenesis. Aberrant miR-130b expression has been reported in several types of cancers. The aim of the present study was to elucidate the effects of miR-130b on BCa progression. miR‑130b expression in BCa cell lines and tissues was detected using real-time PCR (RT-PCR), and vestigial-like protein 4 (VGLL4) expression in tissue specimens and BCa cells that had been transfected with miR-130b mimics and inhibitors was detected using western blotting. Dual-luciferase reporter assay was performed to confirm whether the VGLL4 gene is a direct target of miR-130b, and in vitro cell function testing, Cell Counting Kit-8 (CCK-8) assay, colony formation assay, wound healing and Transwell assays were performed to examine BCa cell proliferation, migration and invasion ability after the cells were transfected with miR-130b mimics and inhibitors and VGLL4 siRNA. miR-130b was found to be upregulated in BCa cells and tissues. miR-130b overexpression promoted BCa cell proliferation, migration and invasion, whereas miR-130b inhibition had the opposite effects. Dual-luciferase reporter assay confirmed that the VGLL4 gene was a direct target of miR-130b and that VGLL4 suppression was crucial for miR‑130b-induced BCa cell proliferation, migration and invasion. The present study showed that miR-130b was significantly upregulated in BCa and may play an oncogenic role in BCa occurrence and development by targeting VGLL4. miR-130b may be a potential therapeutic target in the treatment of BCa.

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