Effects of overexpression of IncRNA AC079466.1 on apoptosis of NSCLC cells through endoplasmic reticulum stress signaling pathway / 中国药理学通报

ABSTRACT

Aim To investigate the expression of IncRNA AC079466. 1 in non-small cell lung cancer (NSCLC) tissues and cells, and the effect of its overexpression on the proliferation, apoptosis, migration and invasion of A549 and H1299 cells. Methods Cancer tissues and corresponding adjacent tissues from 20 NSCLC patients were collected, and the expression of IncRNA AC079466. 1 in tissue and cells was detected by qRT-PCR. AC079466. 1 group was transfected with overexpression plasmid, NC group was transfected with empty plasmid, and no transfection was used in the Blank group. MTT, flow cytometry and Transwell were used to detect the effects of IncRNA AC079466. 1 overexpression on the viability, apoptosis, migration and invasion of A549 and HI299 cells. Western blot was used to detect the effect of overexpression of IncRNA AC079466. 1 on the expression of endoplasmic reticulum stress-related factors GRP78, PERK, eIF2a, ATF4, CHOP, Bax and caspase-3. Results Compared with adjacent tissues, the expression of IncRNA AC079466. 1 in cancer tissues significantly decreased. Compared with HBE cells, the expression of IncRNA AC079466. 1 significantly decreased in A549 and H1299 cells. Compared with the Blank group and NC group, the viability, migration and invasion abilities of A549 and H1299 cells in AC079466. 1 group all markedly decreased, the apoptosis rate apparently increased, and the expressions of endoplasmic reticulum stress-related factors GRP78, p-PERK, eIF2a, ATF4, CHOP, Bax and caspase-3 were significantly up-regulated. Conclusion The overexpression of IncRNA AC079466. 1 significantly inhibits the viability, migration and invasion of A549 and HI299 cells, and promotes cell apoptosis. The mechanism may be related to the promotion of endoplasmic reticulum stress-mediated cell apoptosis.