Open Access
Vitexin induces G2/M‑phase arrest and apoptosis via Akt/mTOR signaling pathway in human glioblastoma cells
Author(s) -
Guangning Zhang,
Dongyuan Li,
Hao Chen,
Junchen Zhang,
Xiaofei Jin
Publication year - 2018
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2018.8394
Subject(s) - vitexin , pi3k/akt/mtor pathway , protein kinase b , cell cycle , apoptosis , cancer research , cell growth , biology , cell cycle checkpoint , viability assay , cancer cell , mechanistic target of rapamycin , cancer , biochemistry , genetics , flavonoid , antioxidant
Glioblastoma is a common primary brain tumor with aggressive malignancy, which results in poor outcomes, short survival time and high mortality. Vitexin, an active ingredient from natural products, has been reported to inhibit cell growth and induce cell apoptosis in various cancer cell lines including hepatocellular carcinoma, oral and esophageal cancer. To the best of the authors knowledge, the present study was the first to investigate anticancer effects of vitexin on human glioblastoma cells and potential underlying mechanisms. The present study demonstrated that vitexin inhibited cell viability in a dose‑ and time‑dependent manner. In the present study, vitexin induced G2/M cell cycle arrest, as demonstrated by flow cytometry. Induction of cell apoptosis following vitexin treatment, was further indicated by observation of morphological alterations, flow cytometry analysis and detection of cleaved‑poly (ADP‑ribose) polymerase. The present study also demonstrated that vitexin inhibited RAC‑alpha serine/threonine‑protein kinase (Akt)/mechanistic target of rapamycin kinase (mTOR) signaling in human glioblastoma cells. Collectively, the results of the present study demonstrated that vitexin induced G2/M cell cycle arrest and apoptosis by inhibiting Akt/mTOR signaling in human glioblastoma cells. Vitexin may in the future be used as a therapeutic agent for treatment of malignant glioblastoma.