Open AccessEffects of miR‑93 on epithelial‑to‑mesenchymal transition and vasculogenic mimicry in triple‑negative breast cancer cells
Author(s) -
Gaili An,
Feng Lu,
Shangke Huang,
Jun Bai,
Li He,
Yi Liu,
Ling Hou
Publication year - 2020
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2020.11668
Subject(s) - vasculogenic mimicry , epithelial–mesenchymal transition , vimentin , gene knockdown , cancer research , triple negative breast cancer , biology , microrna , oncogene , metastasis , angiogenesis , cell migration , breast cancer , cancer , cell , cell cycle , apoptosis , immunology , gene , immunohistochemistry , genetics
Triple‑negative breast cancer (TNBC) is characterized by strong invasiveness, frequent local recurrence and distant metastasis, with poor prognosis. According to tumor angiogenesis theory, tumor cells can obtain blood supply not only by fusing with host blood vessels, but also by constructing a new vascular system through angiogenesis, so as to continuously obtain nutrients and oxygen supply; this is called vasculogenic mimicry (VM). In our previous study, differential expression profiles of miRNAs were examined with gene chip in TNBC and corresponding paracancer tissues, which demonstrated significant up‑regulation of microRNA (miR)‑93. Bioinformatics found that the target genes of miR‑93 were associated with cell proliferation, invasion and migration. The present study investigated the association between miR‑93, epithelial‑to‑mesenchymal transition (EMT) and VM formation in TNBC cell lines. The results indicated that miR‑93 depletion suppressed MDA‑MB‑231 cell viability, invasion and migration (P<0.001). In addition, knockdown of miR‑93 significantly upregulated the expression levels of EMT‑associated genes such as E‑cadherin and occludin, but downregulated the expression levels of vimentin and N‑cadherin in MDA‑MB‑231 cells. VM formation assay showed a significant decrease in microtubule‑forming ability of cells following miR‑93 knockdown, which was associated with the occurrence of EMT, suggesting that miR‑93 may promote the formation of VM via EMT and may be a therapeutic target for the treatment of TNBC.