Open AccessModulation of lncRNA H19 enhances resveratrol‐inhibited cancer cell proliferation and migration by regulating endoplasmic reticulum stress
Author(s) -
Li Tianye,
Zhang Xinyue,
Cheng Linglin,
Li Chunting,
Wu Zihan,
Luo Yingqi,
Zhou Kunpeng,
Li Yanlin,
Zhao Qi,
Huang Yongye
Publication year - 2022
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.17242
Subject(s) - resveratrol , endoplasmic reticulum , gene knockdown , autophagy , unfolded protein response , apoptosis , cell growth , chemistry , thapsigargin , tunicamycin , cancer research , microbiology and biotechnology , cell , programmed cell death , biology , biochemistry
The phytoalexin resveratrol exhibits anti‐tumour activity in many types of cancer. In this study, we showed that resveratrol suppressed the survival of gastric tumour cells both in vivo and in vitro. Resveratrol promoted apoptosis, autophagy and endoplasmic reticulum (ER) stress in a dose‐dependent manner. RNA‐seq analysis showed that multiple cell death signalling pathways were activated after resveratrol treatment, while the use of ER stress activators (tunicamycin and thapsigargin) in combinatorial with resveratrol led to further inhibition of cancer cell survival. Results also showed that resveratrol altered the expression of several long non‐coding RNAs (lncRNAs), including MEG3, PTTG3P, GAS5, BISPR, MALAT1 and H19. Knockdown of H19 in resveratrol‐treated cells further enhanced the effects of resveratrol on apoptosis, ER stress and cell cycle S‐phase arrest. Furthermore, the migratory ability of resveratrol‐treated cells was dramatically decreased after H19 knockdown. In conclusion, resveratrol inhibited cancer cell survival, while knockdown of lncRNA H19 resulted in increased sensitivity to resveratrol therapy.