In vivo and in vitro effects of hyperplasia suppressor gene on the proliferation and apoptosis of lung adenocarcinoma A549 cells

Abstract

Lung adenocarcinoma is the most common subtype of non-small cell lung cancer (NSCLC). Hyperplasia suppressor gene (HSG) has been reported to inhibit cell proliferation, migration, and remodeling in cardiovascular diseases. However, there lacks systematic researches on the effect of HSG on the apoptosis and proliferation of lung adenocarcinoma A549 cells and data of in vivo experiments. The present study aims to investigate the effects of HSG gene silencing on proliferation and apoptosis of lung adenocarcinoma A549 cells. The human lung adenocarcinoma A549 cell was selected to construct adenovirus vector. Reverse transcription-quantitative PCR (RT-qPCR) and Western blot analysis were conducted to detect expressions of HSG and apoptosis related-proteins. Cell Counting Kit (CCK)-8 assay was performed to assess A549 cell proliferation and flow cytometry to analyze cell cycle and apoptosis rate. The BALB/C nude mice were collected to establish xenograft model. Silenced HSG showed decreased mRNA and protein expressions of HSG, and elevated A549 cell survival rates at the time point of 24, 48, and 72 h. The ratio of cells at G0/G1 phase and apoptosis rate decreased and the ratio of cells at S- and G2/M phases increased following the silencing of HSG. There were decreases of B cell lymphoma-2 (Bcl-2)-associated X protein (Bax), Caspase-3, and Caspase-8 expressions but increases in Bcl-2 induced by silenced HSG. As for the xenograft in nude mice, tumor volume increased, and apoptosis index (AI) decreased after HSG silencing. These results indicate that HSG gene silencing may promote the proliferation of A549 cells and inhibit the apoptosis. HSG may be a promising target for the treatment of lung adenocarcinoma.

Ropivacaine inhibits proliferation, invasion, migration and promotes apoptosis of papillary thyroid cancer cells via regulating ITGA2 expression

“…Apoptosis is a programmed cell death involved in numerous physiological and pathological processes, which can help safeguard the genomic integrity. Bcl-2 and Bax, two key proteins of Bcl-2 family, played inverse roles in the regulation of apoptosis as an anti-apoptosis gene and a pro-apoptosis gene, respectively (Ma et al, 2017;Sun, Chen, Guo, Li, & Wang, 2018). In addition, it has been well documented that caspase family proteins, including caspase-3 and caspase-9, are prominent regulators during different phases of the apoptotic pathway (Sun et al, 2010).…”

Overexpression of the hyperplasia suppressor gene inactivates airway fibroblasts obtained from a rat model of chronic obstructive pulmonary disease by inhibiting the Wnt signaling pathway

“…The hyperplasia suppressor gene (HSG) can inhibit cell proliferation and the cell cycle (6,7). HSG is reportedly highly expressed in normal cells, with reduced expression in proliferating cells (8–10).…”

MFN2 deficiency affects calcium homeostasis in lung adenocarcinoma cells via downregulation of UCP4

“…Moreover, the activity of MFN2 is strictly tissue‐ and tumor‐specific and has completely different effects in different cancers. In lung adenocarcinoma, some studies have implicated MFN2 in exerting tumor‐promoting effects [ 8 , 9 ], whereas tumor‐suppressing effects of MFN2 have also been reported [ 10 , 11 , 12 ]. Hence, no consistent conclusion regarding the functions of MFN2 in LUAD has been reached.…”