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Extracellular 5′‐nucleotidase (CD73) promotes human breast cancer cells growth through AKT/GSK‐3β/β‐catenin/cyclinD1 signaling pathway
Author(s) -
Yu Jiangang,
Wang Xue,
Lu Qi,
Wang Jigang,
Li Luying,
Liao Xiaohong,
Zhu Wei,
Lv Lei,
Zhi Xiuling,
Yu Jerry,
Jin Yiting,
Zou Qiang,
Ou Zhouluo,
Liu Xiuping,
Zhou Ping
Publication year - 2017
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.31112
Subject(s) - protein kinase b , cancer research , cell growth , breast cancer , pi3k/akt/mtor pathway , biology , 5' nucleotidase , adenosine , signal transduction , cancer , chemistry , endocrinology , microbiology and biotechnology , medicine , biochemistry
To identify the role and to explore the mechanism of extracellular 5′‐nucleotidase (CD73) in human breast cancer growth, CD73 expression was measured firstly in breast cancer tissues and cell lines, and then interfered with or over‐expressed by recombinant lentivirus in cell lines. Impacts of CD73 on breast cancer cell proliferation and cell cycle were investigated with colony formation assay, CCK‐8 and flow cytometry. The relationship between CD73 and AKT/GSK‐3β/β‐catenin pathway was assessed with adenosine, adenosine 2A receptor antagonist (SCH‐58261), adenosine 2A receptor agonist (NECA), CD73 enzyme inhibitor (APCP) and Akt inhibitor (MK‐2206). Moreover, the effect of CD73 on breast cancer growth in vivo was examined with human breast cancer transplanting model of nude mice. The results showed that the expression of CD73 was high in breast cancer tissues and increased with advanced tumor grades and lympho‐node status. CD73 expression was higher in more malignant cells, and CD73 overexpression promoted breast cancer cell proliferation in both in vivo and in vitro . It activated AKT/GSK‐3β/β‐catenin/cyclinD1 signaling pathway through CD73 enzyme activity and other mechanism.