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Polydatin inhibits cell proliferation and induces apoptosis in laryngeal cancer and HeLa cells via suppression of the PDGF/AKT signaling pathway
Author(s) -
Li Haixia,
Shi Baoyuan,
Li Yanyun,
Yin Fengfang
Publication year - 2017
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.21900
Subject(s) - protein kinase b , platelet derived growth factor receptor , hela , apoptosis , cell growth , chemistry , cancer research , signal transduction , flow cytometry , cancer cell , cell cycle , microbiology and biotechnology , cell , biology , growth factor , cancer , receptor , biochemistry , genetics
Polydatin (PD), a stilbene compound extracted from Polygonum cuspidatum , is suggested to possess anti‐cancer activities, including inhibition of cell proliferation, cell cycle arrest, and induction of apoptosis. The platelet‐derived growth factor (PDGF)/AKT signaling pathway plays complex roles in tumor suppression. However, the effect of PD on the PDGF/AKT signaling pathway in laryngeal cancer and HeLa cells has not been explored. MTT assay and flow cytometry showed that PD inhibited cell proliferation and induced apoptosis in Hep‐2 and AMC‐HN‐8 cells. Western blot analysis indicated that PD inhibited the expression levels of PDGF‐B and phosphorylated AKT (p‐AKT) in both cells. Treatment of PDGF‐B siRNA or PDGFR inhibitor found that after the PDGF signaling was inactivated, p‐AKT expression was significantly decreased in Hep‐2 cells. Tumor xenograft experiment in nude mice indicated PD significantly inhibited the growth of Hep‐2 cells in vivo . In conclusion, PD inhibited cell proliferation and induced apoptosis in laryngeal cancer and HeLa cells via inactivation of the PDGF/AKT signaling pathway.