Open AccessResveratrol suppresses the growth and metastatic potential of cervical cancer by inhibiting STAT3 Tyr705 phosphorylation
Author(s) -
Sun Xiaodong,
Xu Qianqian,
Zeng Lian,
Xie Lixia,
Zhao Qiang,
Xu Hongxia,
Wang Xuanbin,
Jiang Nan,
Fu Pan,
Sang Ming
Publication year - 2020
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.3510
Subject(s) - stat3 , cancer research , angiogenesis , phosphorylation , stat protein , metastasis , apoptosis , epithelial–mesenchymal transition , resveratrol , biology , hela , signal transduction , western blot , cancer , chemistry , cell , microbiology and biotechnology , pharmacology , biochemistry , genetics , gene
Aberrant signal transducer and activator of transcription 3 (STAT3) signaling promotes the initiation and progression of cancer in humans by either inhibiting apoptosis or inducing cell proliferation, angiogenesis, invasion, and metastasis. The role of resveratrolRESin inhibiting the STAT3 signaling pathway in vivo , particularly in cervical cancer is still unknown. This study aims to investigate the role of STAT3 and its phosphorylation in RES‐mediated suppression of cervical cancer. The effects of RES on cervical cancer were determined by examining tumor tissues, their histological changes, and the volume and weight of tumor tissues grown from HeLa cells injected in female athymic BALB/C nude mice. The structure and target interaction of RES were virtually screened using the molecular docking program Autodock Vina. The status of phosphorylated STAT3, protein levels of epithelial‐mesenchymal transition molecular markers and extracellular matrix degradation enzymes were determined through Western blot. We demonstrated that RES could suppress the proliferation and metastatic potential of cervical cancer cells by inactivating phosphorylation of STAT3 at Tyr705 but not Ser727. This effect was intensified by inhibition of the STAT3 signal pathway.