High mobility group AT-hook 2 promotes tumorigenicity of pancreatic cancer cells via upregulating ANLN

• Published in: Experimental cell research 2020-08, Vol.393 (1), p.112088, Article 112088
• Main Authors: Guo, Hua-Hu, Wang, Ya-Zhou, Zhang, Zheng-Kui, Li, Ming-Zhe, Tian, Xiao-Dong, Yang, Yin-Mo
• Format: Article
• Language: English
• Subjects: Animals; ANLN; Carcinogenesis - genetics; Cell Movement - physiology; Cell Proliferation - physiology; Cell Transformation, Neoplastic - genetics; Gene Expression Regulation, Neoplastic - genetics; HMGA2; HMGA2 Protein - metabolism; Humans; Mice, Nude; Microfilament Proteins - metabolism; Pancreatic cancer; Pancreatic Neoplasms - metabolism; Pancreatic Neoplasms - mortality; Tumorigenicity; Up-Regulation
• ISSN: 0014-4827; 1090-2422
• DOI: 10.1016/j.yexcr.2020.112088

HMGA2 is associated with the regulation of cellular biological processes in various human disorders and cancer progression, yet little is known about how HMGA2 controls tumorigenesis. This study uncovered the mechanism of HMGA2-mediated regulation of tumorigenicity in pancreatic cancer. We showed that HMGA2 was highly expressed in pancreatic cancer cells and correlated with poor prognosis. HMGA2 expression knockdown inhibited the tumorigenicity of pancreatic cancer cells. Conversely, overexpression of HMGA2 promoted tumorigenicity. Combination of ChIP-Seq, RNA-Seq and dual-luciferase reporter assays revealed HMGA2 could directly regulate ANLN expression. Furthermore, we found ANLN could mediate the HMGA2-induced effects on pancreatic cancer cells. The identification of the regulatory mechanism of HMGA2 and ANLN will provide insights into the progression for human pancreatic cancer. [Display omitted] •HMGA2 promoted tumorigenicity of pancreatic cancer cells.•HMGA2 directly regulated ANLN expression by binding promoter region.•ANLN mediated the effect on pancreatic cancer induced by HMGA2.