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S100A2 promotes glycolysis and proliferation via GLUT1 regulation in colorectal cancer
Author(s) -
Li Chen,
Chen Qinbo,
Zhou Yi,
Niu Yan,
Wang Xinyi,
Li Xiang,
Zheng Hong,
Wei Tingting,
Zhao Liangcai,
Gao Hongchang
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.202000555r
Subject(s) - glut1 , reprogramming , cancer research , pi3k/akt/mtor pathway , colorectal cancer , protein kinase b , glycolysis , downregulation and upregulation , akt2 , cancer , biology , signal transduction , glucose transporter , microbiology and biotechnology , gene , endocrinology , metabolism , genetics , akt1 , insulin
The deregulation of S100A2 has been implicated in the pathogenesis of several types of cancers. However, the molecular mechanisms underlying the protumorigenic capacities of S100A2 have not been fully elucidated. Here, we demonstrated the molecular mechanisms underlying the roles of S100A2 in glycolysis reprogramming and proliferation of colorectal cancer (CRC) cells. The results indicated that S100A2 overexpression raises glucose metabolism and proliferation. Mechanistically, S100A2 activated the PI3K/AKT signaling pathway, upregulated GLUT1 expression, induced glycolytic reprogramming, and consequently increased proliferation. Clinical data showed significantly increased S100A2 levels in CRC tissues and the Oncomine database. In addition, analysis revealed a positive correlation between S100A2 and GLUT1 mRNA expression in CRC tissues. Together, these results demonstrate that the S100A2/GLUT1 axis can promote the progression of CRC by modulating glycolytic reprogramming. Our results further suggest that targeting S100A2 could present a promising therapeutic avenue for the prevention of colorectal cancer progression.