Atractylenolide II Inhibits Proliferation, Motility and Induces Apoptosis in Human Gastric Carcinoma Cell Lines HGC-27 and AGS

Abstract

Atractylenolide II (AT-II) exhibits several biological and pharmacological functions, especially anti-cancer activity as the major sesquiterpene lactones isolated from Atractylodes macrocephala (also named Baizhu in Chinese). However, the effects and mechanisms of AT-II on human gastric cancer remain unclear. Cell Counting Kit-8 (CCK-8) assay, morphological changes, flow cytometry, wound healing assay and Western blot analysis were used to investigate the effects of AT-II on cell proliferation, apoptosis and motility of human gastric carcinoma cell lines HGC-27 and AGS. Our results indicated that AT-II could significantly inhibit cell proliferation, motility and induce apoptosis in a dose and time-dependent manner. Western blot analysis showed that the expression level of Bax was upregulated and the expression levels of B-cell lymphoma-2 (Bcl-2), phosphorylated-protein kinase B (p-Akt) and phosphorylated-ERK (p-ERK) were downregulated compared to control group. In conclusion, the findings suggested that AT-II exerted significant anti-tumor effects on gastric carcinoma cells by modulating Akt/ERK signaling pathway, which might shed light on therapy of gastric carcinoma.

Chinese herbal medicine combined with oxaliplatin-based chemotherapy for advanced gastric cancer: A systematic review and meta-analysis of contributions of specific medicinal materials to tumor response

“…A randomized controlled trial also verified the therapeutic effect of AT-1 on GC cachexia ( Liu et al, 2008 ). Similarly, for Atractylenolide II (AT-II), Bax expression could also be up-regulated, and B-cell lymphoma 2 (Bcl-2), phosphorylated protein kinase B (p-Akt), and phosphorylated ERK (p-ERK) expression could be down-regulated, which induced apoptosis and inhibited proliferation and migration of HGC-27 and AGS in a concentration- and time-dependent manner by inactivating Ras/ERK and PI3K/Akt signaling pathways ( Tian et al, 2017 ). AT-1 and AT-2 also inhibit Akt/IκBα/NF-κB signaling pathway to play a role, thereby inhibiting gastritis to GC transformation ( Amin et al, 2022 ).…”

Hispidulin Enhances Temozolomide (TMZ)-Induced Cytotoxicity against Malignant Glioma Cells In Vitro by Inhibiting Autophagy

“…Bcl-2 family members, Bax (proapoptotic) and Bcl-2 (antiapoptotic), are critical in the regulation of apoptotic cell death [ 19 , 20 ]. A change of the Bax/Bcl-2 ratio is known to ultimately activate the caspase family of proteins, such as caspase-9 and caspase-3 [ 18 ].…”

“…U87MG cells were seeded into each well at a density of 2 × 10 5 cells/mL in a 96well microplate. After 24 h, cells were suspended in the medium containing different concentrations of hispidulin (5,10,20,40, and 100 μg/ml), TMZ (50, 100, 200, 400, and 800 μM), or their combination TMZ (100 μg/ml of TMZ and 100 μg/ml of hispidulin) for 48 h. en, the cells were washed with PBS, and 10 μL MTT (5 mg/ml) was added to each well. Following 4 h incubation at 37 °C, the supernatant was discarded, and the formed formazan crystals in viable cells were lysed by adding DMSO (100 μl) in each well.…”

Atractylenolide III induces apoptosis by regulating the Bax/Bcl-2 signaling pathway in human colorectal cancer HCT-116 Cells in vitro and in vivo

“…Its main active ingredients include atractylenolide I, II and III [13]. Numerous studies have shown that atractylenolide I and II exhibited obvious anticancer and chemopreventive activities by significantly inhibiting the cell proliferation and inducing apoptosis and cell cycle arrest in various cancer cells [14][15][16][17][18][19]. However, the study is limited for the anticancer effect of atractylenolide III.…”