HMGB1 Promotes the Proliferation and Metastasis of Lung Cancer by Activating the Wnt/β-Catenin Pathway

The aim of this study was to investigate the role of high mobility group protein-1 (HMGB1) in the proliferation and migration of lung cancer cells. CCK-8 assays and colony formation assays were used to evaluate the effect of HMGB1 regulation on cancer cell viability and colony formation. Trans-well...

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Bibliographic Details
Published in:Technology in cancer research & treatment 2020, Vol.19, p.1533033820948054
Main Authors: Wang, Xiao-hui, Zhang, Shu-ying, Shi, Mei, Xu, Xiao-peng
Format: Article
Language:English
Subjects:
Cell migration
Cell proliferation
Cell viability
Cholecystokinin
Colonies
High mobility group proteins
HMGB1 protein
Lung cancer
Mesenchyme
Metastases
Motility
Original
Tumor cell lines
Western blotting
Wnt protein
Wound healing
β-Catenin
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Summary:The aim of this study was to investigate the role of high mobility group protein-1 (HMGB1) in the proliferation and migration of lung cancer cells. CCK-8 assays and colony formation assays were used to evaluate the effect of HMGB1 regulation on cancer cell viability and colony formation. Trans-well assays and wound healing assays were also performed. Our data showed that HMGB1 is upregulated in clinical lung cancer tissues compared with non-cancer tissues, and it is differentially expressed in lung cancer cell lines. The knockdown of HMGB1 in A549 lung cancer cells significantly reduced cell proliferation, viability and motility. In contrast, overexpression of HMGB1 in lung cancer H1299 cells significantly increased cell viability and motility. Western blotting showed that HMGB1 could promote epithelial-mesenchymal transition. The Wnt/β-catenin pathway was activated after overexpression of HMGB1 in H1299 cells, while it was inactivated by knocking down HMGB1 in A549 cells. These data suggest that HMGB1 promotes the proliferation and migration of lung cancer cells in vitro. The carcinogenic behavior of HMGB1 can be achieved by activating the Wnt/β-catenin pathway.
ISSN:1533-0346
1533-0338
DOI:10.1177/1533033820948054