癌症研究
癌症
粒体自噬
癌细胞
细胞生长
PVT1型
甲基化
DNA甲基化
生物
转移
蛋氨酸
下调和上调
化学
自噬
DNA去甲基化
细胞凋亡
长非编码RNA
DNA
生物化学
基因表达
遗传学
基因
氨基酸
作者
Lin Xin,Hao Lü,Chuan Liu,Fei Zeng,Yi‐Wu Yuan,You Wu,Jinliang Wang,Deng-Zhong Wu,Liqun Zhou
标识
DOI:10.1016/j.biocel.2021.106100
摘要
The occurrence of recurrence and metastasis after treatment is a major challenge in the treatment of gastric cancer. This study was based on the methionine (Met)-dependent characteristics of gastric cancer cells to explore the effect of Met deficiency on the occurrence and development of gastric cancer.Human gastric cancer cell lines MKN45 and AGS and nude mice model were used to explore how Met affects gastric cancer by regulating lncRNA PVT1.The levels of lncRNA PVT1 in gastric cancer cells and human gastric cancer xenografts of nude mice were down-regulated under the condition of Met deficiency. The cell viability and cell proliferation were declined after MKN45 and SGC-790 cells were cultured in Met-deficient medium. LncRNA PVT1 could affect BNIP3 promoter DNA methylation level through its interaction with DNMT1. Moreover, the silence of lncRNA PVT1 and the up-regulation of BNIP3 level inhibited the gastric cancer cell proliferation. Met deficiency could up-regulate BNIP3 expression by inhibiting the binding of lncRNA PVT1 to DNMT1, and activate mitophagy, thus inhibiting gastric cancer cell proliferation.Our study suggested that Met deficiency could down-regulate the expression of lncRNA PVT1, further demethylated the promoter of BNIP3, thus inhibiting the proliferation of gastric cancer cells by activating mitophagy.
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