Long non-coding RNA VIM-AS1 is upregulated in high-grade invasive ductal breast tumors and promotes breast cancer metastasis via inducing EMT

Abstract

Long non-coding RNAs (lncRNAs) are established as vital biological regulators in various important cellular mechanisms and diseases. They aren't able to encode proteins and their length is longer than 200 nucleotides. VIM-AS1, as a lncRNA, is transcribed from the common bidirectional promoter with Vimentin and positively regulated Vimentin expression via forming a stable R-loop structure in its promoter region. In present study intended to find the relative expression of VIM-AS1 in breast cancer (BC) compared with their corresponding non-tumor samples employing RT-qPCR. Furthermore, knocking down experiments was employed to decipher the functional role of VIM-AS1 in BC cells. Moreover, we assessed the impact of VIM-AS1 suppressing on different cellular processes including cell cycle, apoptosis, colony formation ability, cellular senescence, and EMT. We observed VIM-AS1 was only expressed in high-grade ductal BC and its expression has a positive correlation with lymphatic metastasis of BC cells. RNA interference-mediated suppression experiments showed that VIM-AS1 knocking down not only suppressed cancer cell proliferation but also triggered G2/M cell cycle arrest, apoptosis, and cellular senescence in high-grade BC -derived cells. Additionally, we found that VIM-AS1 enhanced cell migration via inducing the epithelial to mesenchymal transition (EMT). Together, the findings suggest that VIM-AS1 upregulation may contribute to progress and metastasis of BC cells via regulating EMT and it can be noticed as a probable biomarker for diagnosis and prognosis of high-grade BC.