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HMGB1 knock‐down promoting tumor cells viability and arrest pro‐apoptotic proteins via Stat3/NFκB in HepG2 cells
Author(s) -
Alduais Salah,
Alduais Yaser,
Wu Xiaolei,
Li Haosen,
Mao Jing
Publication year - 2018
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.1456
Subject(s) - apoptosis , hmgb1 , viability assay , gene silencing , annexin , microbiology and biotechnology , stat3 , transfection , cancer research , signal transduction , flow cytometry , small interfering rna , biology , western blot , inflammation , chemistry , cell culture , immunology , biochemistry , genetics , gene
Background/Aim: High mobility group box 1 protein (HMGB1) is functionally dynamic and pleiotropic molecule, it has the potential to promote both cell survival and death by regulating multiple signaling pathways, including inflammation and apoptosis. This study aimed at investigating the role of silencing HMGB1 on tumor cells apoptosis and pro‐inflammatory proteins expression in hepatocellular HepG2 cancer cells. Methods: HepG2 cells was transfected with si‐RNA HMGB1, and the effect on pro‐apoptotic proteins expressions like Bax, Bcl2, and pro‐inflammatory cytokines like, p65‐NFκB, and Cyclooxygenase‐2 (Cox2) was assessed using western blot, and also cells apoptosis and proliferation was assessed using annexin V FITC and Calcien AM expression in flow cytometry and fluorescence. Results: HMGB1 silencing was found significantly increase tumor cells viability with significant decrease of pro‐apoptotic proteins, also antiapoptotic protein Bcl2 was significantly up‐regulated, which suggests a possible role in restricting apoptosis. Furthermore, HMGB1 knocked down found to inhibit Stat3 phosphorylation and significantly affect NFkB p65/Cox2 expression which suggests a link between HMGB1 and Stat3 activation. Our results revealed that HMGB1 knocked down may suppress cells apoptosis and enhance HepG2 cells viability via NFkB/Cox2 and Stat3. © 2018 BioFactors, 44(6):570–576, 2018