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Leukemia inhibitory factor promotes tumor growth and metastasis in human osteosarcoma via activating STAT 3
Author(s) -
Liu Bin,
Lu Yi,
Li Jinzhi,
Liu Yanping,
Liu Jian,
Wang Weiguo
Publication year - 2015
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/apm.12427
Subject(s) - osteosarcoma , leukemia inhibitory factor , cancer research , stat3 , oncogene , in vivo , metastasis , leukemia , gene knockdown , cancer , medicine , phosphorylation , chemistry , biology , cell culture , cell cycle , cytokine , microbiology and biotechnology , interleukin 6 , genetics
The leukemia inhibitory factor ( LIF ) has been demonstrated to be an oncogene and participated in multiple procedures during the initiation and progression of many human malignancies. However, the role of LIF in osteosarcoma is still largely unknown. Here, we performed a series of in vitro and in vivo experiments to investigate the expression and biological functions of LIF in osteosarcoma. Compared to that in the non‐cancerous tissues, LIF was significantly overexpressed in a panel of 68 osteosarcoma samples (p < 0.0001). Moreover, the overexpression of LIF was significantly correlated with advanced tumor stage, larger tumor size, and shorter overall survival. In addition, knockdown of LIF notably suppressed the proliferation and invasion of osteosarcoma via blocking the STAT 3 signal pathway; in contrast, treatment with the recombinant LIF protein significantly promoted the growth and invasion of osteosarcoma through enhancing the phosphorylation of STAT 3, which can be partially neutralized by the STAT 3 inhibitor, HO ‐3867. In conclusion, we demonstrated that LIF was frequently overexpressed in osteosarcoma, which could promote the growth and invasion through activating the STAT 3 pathway. Our findings proposed that LIF might be a potent therapeutic target for osteosarcoma.