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Diallyl disulfide antagonizes DJ‐1 mediated proliferation, epithelial–mesenchymal transition, and chemoresistance in gastric cancer cells
Diallyl disulfide (DADS), an organic component of allicin abstracted from garlic, possesses multi‐target antitumor activity. DJ‐1 performs a vital function in promoting AKT aberrant activation via down‐regulating phosphatase and tensin homologue (PTEN) in tumors. It is unknown the involvement of DJ‐1 in epithelial–mesenchymal transition (EMT) of gastric cancer (GC) cells. The purpose of this study is to investigate whether diallyl disulfide (DADS) intervenes in the role of DJ‐1 in GC. Based on the identification that the correlation between high DJ‐1 and low PTEN expression in GC was implicated in clinical progression, we illuminated that down‐regulation of DJ‐1 by DADS aided in an increase in PTEN expression and a decrease in phosphorylated AKT levels, which was in line with the results manifested in the DJ‐1 knockdown and overexpressed cells, concurrently inhibiting proliferation, EMT, migration, and invasion. Furthermore, the antagonistic effects of DADS on DJ‐1 were observed in in vivo experiments. Additionally, DADS mitigated the DJ‐1‐associated drug resistance. The current study revealed that DJ‐1 is one of potential targets for DADS, which hopefully provides a promising strategy for prevention and adjuvant chemotherapy of GC.
Diallyl disulfide antagonizes DJ‐1 mediated proliferation, epithelial–mesenchymal transition, and chemoresistance in gastric cancer cells
Diallyl disulfide (DADS), an organic component of allicin abstracted from garlic, possesses multi‐target antitumor activity. DJ‐1 performs a vital function in promoting AKT aberrant activation via down‐regulating phosphatase and tensin homologue (PTEN) in tumors. It is unknown the involvement of DJ‐1 in epithelial–mesenchymal transition (EMT) of gastric cancer (GC) cells. The purpose of this study is to investigate whether diallyl disulfide (DADS) intervenes in the role of DJ‐1 in GC. Based on the identification that the correlation between high DJ‐1 and low PTEN expression in GC was implicated in clinical progression, we illuminated that down‐regulation of DJ‐1 by DADS aided in an increase in PTEN expression and a decrease in phosphorylated AKT levels, which was in line with the results manifested in the DJ‐1 knockdown and overexpressed cells, concurrently inhibiting proliferation, EMT, migration, and invasion. Furthermore, the antagonistic effects of DADS on DJ‐1 were observed in in vivo experiments. Additionally, DADS mitigated the DJ‐1‐associated drug resistance. The current study revealed that DJ‐1 is one of potential targets for DADS, which hopefully provides a promising strategy for prevention and adjuvant chemotherapy of GC.
Diallyl disulfide antagonizes DJ‐1 mediated proliferation, epithelial–mesenchymal transition, and chemoresistance in gastric cancer cells
Su, Jian (Autor:in) / Xia, Hong (Autor:in) / He, Hui (Autor:in) / Tang, Huan (Autor:in) / Zhou, Juan (Autor:in) / Xun, Yi (Autor:in) / Liu, Fang (Autor:in) / Su, Bo (Autor:in) / Su, Qi (Autor:in)
Environmental Toxicology ; 39 ; 4105-4119
01.08.2024
15 pages
Aufsatz (Zeitschrift)
Elektronische Ressource
Englisch
| Wiley | 2023
Metabolic reprogramming and epithelial‐to‐mesenchymal transition in cancer
| British Library Online Contents | 2017