ArticleTranslational cancer research2019
Acid-induced autophagy protects human gastric cancer cells from apoptosis by activating Erk1/2 pathway.
Article in Translational cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- NSUN6 Promotes Gastric Cancer Progression by Stabilizing CEBPZ mRNA in a mApplied biochemistry and biotechnology · 2025Article
- Potential mechanism of traditional Chinese medicine intervention in gastric cancer: targeted regulation of autophagy.Frontiers in pharmacology · 2025Review
- LC3B, mTOR, AMPK Are Molecular Targets for Neoadjuvant Chemotherapy in Gastric Cancers.Current issues in molecular biology · 2022Article
- Silencing c-Jun inhibits autophagy and abrogates radioresistance in nasopharyngeal carcinoma by activating the PI3K/AKT/mTOR pathway.Annals of translational medicine · 2021Article
- MicroRNA-153-3p sensitizes melanoma cells to dacarbazine by suppressing ATG5-mediated autophagy and apoptosis.Translational cancer research · 2020Article
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6 authors.
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Abstract
backgroundAcidic microenvironments exist widely in tumors. However, the specific mechanism of cancer cell survival under an acidic microenvironment remains unknown. This study aims to investigate whether acid can induce autophagy and examine the mechanism of autophagy in gastric cancer cells.
methodsHuman gastric adenocarcinoma (AGS) cells were cultured in media with different pH values
resultsWe found that the protein expression of autophagy markers such as LC3II/I and Beclin1 was higher in AGS cells treated with an acidic microenvironment than in control cells. The protein expression level of P62 was obviously decreased in acid-treated cells compared to that in control cells. Furthermore, the expression of Erk1/2 pathway markers, including p-Erk1/2, was also increased in response to acidic pH. Dense LC3 puncta were observed in cells cultured under acidic conditions, whereas untreated cells exhibited diffuse and weak LC3 puncta; an increased autophagy flux could also be observed. The presence of autophagosomes was observed by TEM in AGS cells subjected to low pH. Additionally, autophagy was inhibited by the autophagy inhibitor Bafilomycin A1 (Baf) and apoptosis was obviously increased. Moreover, cells exposed to an acidic microenvironment displayed facilitated growth compared with that in control cells.
conclusionsTaken together, these results indicate that the acidic microenvironment promotes AGS cell growth by upregulating autophagy through the Erk1/2 pathway, which acts as a survival adaptation.
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