Knockdown of LncRNAZFAS1 suppresses cell proliferation and metastasis in non-small cell lung cancer

Abstract

To evaluate the effects of LncRNAZFAS1 on cell proliferation and tumor metastasis in non-small cell lung cancer (NSCLC), we detected the expression level of LncRNAZFAS1 in NSCLC-related tissues and cells. qRT-PCR results revealed that LncRNAZFAS1 in tumor tissues was significantly higher than that in normal lung tissue, especially significantly up-regulated in stage III / IV and in metastatic NSCLC tissues. LncRNAZFAS1 expression was dramatically up-regulated in 4 NSCLCrelated cells (A549, SPC-A1, SK-MES-1, and NCI-H1299), with having the highest expression level in A549 cells. Furthermore, we implemented a knockdown of LncRNAZFAS1 in A549 cells, and the results of CCK8 and Transwell assays suggested that knockdown of LncRNAZFAS1 significantly inhibited NSCLC cell proliferation and metastasis. Next, we constructed a tumor xenograft model to evaluate the effect of LncRNAZFAS1 on the NSCLC cell proliferation in vivo. The results indicated that knockdown of LncRNAZFAS1 dramatically inhibited A549 cells proliferation and repressed tumor growth. Additionally, knockdown of LncRNAZFAS1 drastically weakened the expressions of MMP2, MMP9 and Bcl-2 proteins, whereas noticeably strengthened the expression of BAX protein. Our results altogether suggest that knockdown of LncRNAZFAS1 has a negative effect on the proliferation and metastasis of NSCLC cell, which implying LncRNAZFAS1 is a potential unfavorable biomarker in patients with NSCLC.

Human Endogenous Retroviruses: Friends and Foes in Urology Clinics

“…HERV sequences in the genome can serve as regulatory elements that affect gene expression by interacting with various transcription factors (TFs), including some key players in physiological and pathological processes [14]. Also, failure to repress HERVs or their dysregulated expression is associated with numerous human diseases and disorders, including various cancers and infertility, which involve many critical molecular, cellular, and physiological pathways [15][16][17][18][19][20][21]. The unwanted activation of HERVs can be induced by inflammation, endocrine imbalance, exogenous viral infections, chemical exposures, and other environmental conditions [4,[22][23][24].…”

UCH-L1 and UCH-L3 regulate the cancer stem cell-like properties through PI3 K/Akt signaling pathway in prostate cancer cells

“…Recent studies have proposed that EMT induces CSC-like features in cancer cells. During cancer development, activation of the EMT program increases the tumor initiation capacity and imparts cancer cells with resistance to a range of therapeutic agents (Shibue and Weinberg 2017 ; Zhou et al 2020 ). Previously, the EMT regulation of prostate cancer cells by UCH-L1 and UCH-L3 was reported (Jang et al 2011 ; Song et al 2014 ).…”