Schizandrin A induces the apoptosis and suppresses the proliferation, invasion and migration of gastric cancer cells by activating endoplasmic reticulum stress
- Huachao Pu
- Qian Qian
- Fuli Wang
- Minjie Gong
- Xinguo Ge
Affiliations: Department of Oncology, Changzhou Hospital of Traditional Chinese Medicine, Changzhou, Jiangsu 213000, P.R. China, Department of Gastroenterology, The First People's Hospital of Changzhou (The Third Affiliated Hospital of Soochow University), Changzhou, Jiangsu 213000, P.R. China, Department of Oncology, Changzhou Jin Dongfang Hospital, Changzhou, Jiangsu 213000, P.R. China
- Published online on: September 9, 2021 https://doi.org/10.3892/mmr.2021.12427
Copyright: © Pu
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Apart from its basic antioxidant and anti‑inflammatory properties, schizandrin A (SchA), which is isolated from Fructus schisandra, can exert anticancer effects on multiple cancer types. However, to the best of our knowledge, there has been no study identifying the impacts of SchA on gastric cancer (GC). Therefore, the aim of the present study was to identify how SchA functioned to affect the progression of GC. To investigate the role of SchA in GC development, Cell Counting Kit‑8, colony formation, wound healing and Transwell assays were conducted to assess the viability, proliferation, migration and invasion of AGS cells, respectively. Then, the apoptosis rate and apoptosis‑ and endoplasmic reticulum (ER) stress‑related protein expression levels in AGS cells exposed to SchA were detected via TUNEL assays and western blotting, respectively. Subsequently, the aforementioned functional assays were performed again in AGS cells exposed to both SchA and the ER stress inhibitor 4‑phenylbutyric acid (4‑PBA) for the confirmation of the effect of SchA on ER stress in GC. It was found that SchA markedly decreased the viability, proliferation, migration and invasion, while it induced the apoptosis of AGS cells. Moreover, the markers of ER stress were elevated by SchA treatment in AGS cells. Nevertheless, 4‑PBA reversed the effects of SchA on the viability, proliferation, migration, invasion and apoptosis of AGS cells, accompanied by decreased expression of ER stress markers. In conclusion, the present study demonstrated that SchA induced the apoptosis and suppressed the proliferation, invasion and migration of GC cells by activating ER stress, which provides a theoretical basis for the use of SchA in the treatment of GC.