ArticleCell death & disease2019
Inhibiting lysine 353 oxidation of GRP78 by a hypochlorous probe targeting endoplasmic reticulum promotes autophagy in cancer cells.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 28 citations in OpenAlex.
- Integrating molecular generation and fingerprints transferring for single-molecule theranostics targeting endoplasmic reticulum stress.Journal of advanced research · 2026Article
- Advances in endogenous hypochlorous acid-mediated regulation of tumor cell fates.Frontiers in cell and developmental biology · 2026Review
- Inhibition of PERK-eIF2α-ATF4 signaling enhances the antiviral effects of resveratrol-loaded nanoparticles against enterovirus 71 in hand, foot, and mouth disease.Archives of virology · 2025Article
- Activation of GRP78 ATPase suppresses A549 lung cancer cell migration by promoting ITGB4 degradation.Cell adhesion & migration · 2022Article
- Identification of a new way to induce differentiation of dermal fibroblasts into vascular endothelial cells.Stem cell research & therapy · 2022Article
- Article
- Hypochlorous Acid: From Innate Immune Factor and Environmental Toxicant to Chemopreventive Agent Targeting Solar UV-Induced Skin Cancer.Frontiers in oncology · 2022Review
- Topical hypochlorous acid (HOCl) blocks inflammatory gene expression and tumorigenic progression in UV-exposed SKH-1 high risk mouse skin.Redox biology · 2021Article
- GRP78 in lung cancer.Journal of translational medicine · 2021Review
- SOCS3 Negatively Regulates Cardiac Hypertrophy via Targeting GRP78-Mediated ER Stress During Pressure Overload.Frontiers in cell and developmental biology · 2021Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The level of hypochlorous acid (HOCl) in cancer cells is higher than that in non-cancer cells. HOCl is an essential signal for the regulation of cell fate and works mainly through the protein post-translational modifications in cancer cells. However, the mechanism of HOCl regulating autophagy has not been clarified. Here we reported that a HOCl probe named ZBM-H targeted endoplasmic reticulum and induced an intact autophagy flux in lung cancer cells. Furthermore, ZBM-H promoted the binding of GRP78 to AMPK and increased the phosphorylation of AMPK in a dose- and time-dependent manner. GRP78 knockdown inhibited ZBM-H-induced AMPK phosphorylation and ZBM-H-stimulated autophagy. In addition, mass spectrometry combined with point mutation experiments revealed that ZBM-H increased GRP78 activity by inhibiting HOCl-induced lysine 353 oxidation of GRP78. Following ZBM-H treatment in vitro and in vivo, cell growth was significantly inhibited while apoptosis was induced. Nevertheless, exogenous HOCl partially reversed ZBM-H-inhibited cell growth and ZBM-H-induced GRP78 activation. In brief, we found that an endoplasmic reticulum-targeted HOCl probe named ZBM-H, acting through attenuating HOCl-induced GRP78 oxidation, inhibited tumor cell survival by promoting autophagy and apoptosis. Overall, these data demonstrated a novel mechanism of hypochlorous acid regulating autophagy by promoting the oxidation modification of GRP78.
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