ANP32A promotes the proliferation, migration and invasion of hepatocellular carcinoma by modulating the HMGA1/STAT3 pathway

Author:

Tian Zilu12,Liu Zhiyi12,Fang Xiaokang12,Cao Kuan12,Zhang Bin12,Wu Rui12,Wen Xin12,Wen Quan12,Shi Hengliang123ORCID,Wang Renhao12

Affiliation:

1. Institute of Digestive Diseases, The Affiliated Hospital of Xuzhou Medical University, Xuzhou Medical University, Xuzhou, Jiangsu, China

2. Department of General Surgery, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China

3. Central Laboratory, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China

Abstract

Abstract Acidic leucine-rich nuclear phosphoprotein-32A (ANP32A) has been reported to play an essential role in the development and progression of various human cancers. However, its expression pattern and possible mechanism in human hepatocellular carcinoma (HCC) remain to be elucidated. In this study, we used western blot and immunohistochemical staining to detect protein expression. The effects of ANP32A on the proliferation, migration and invasion of HCC cells were examined using 5-ethynyl-20-deoxyuridine (EdU), colony formation, CCK-8, and transwell assays. RT-qPCR was performed to detect mRNA expression. The interaction between ANP32A and the high mobility group A1 (HMGA1) mRNA was assessed using RNA immunoprecipitation (RIP). The tumorigenicity of ANP32A was assessed by establishing a xenograft tumor model in Balb/c nude mice. We found that the ANP32A protein was expressed at high levels in patients with HCC, which was associated with a poor prognosis. Functional experiments revealed that the silencing of ANP32A inhibited the proliferation, migration, and invasion of HCC cells, whereas overexpression of ANP32A promoted these processes. Further investigations indicated that ANP32A bound the HMGA1 mRNA and maintained its stability to promote the expression of HMGA1, thereby increasing the expression and activation of STAT3. Finally, a xenograft tumor model of Balb/c nude mice confirmed the tumorigenicity of ANP32A. This study found that ANP32A is up-regulated in patients with HCC and may accelerate the proliferation, migration and invasion of HCC cells by modulating the HMGA1/STAT3 pathway.

Funder

Natural Science Foundation of Jiangsu Province of China

National Natural Science Foundation of China

Foundation of Jiangsu Provincial Health Department

Foundation of Xuzhou Science and Technology Bureau

Jiangsu Provincial Qing Lan Project and Jiangsu Provincial Medical Youth Talent

Technology Innovation Team of Xuzhou Medical University Key Research and Development Plan of Jiangsu Province

Publisher

Oxford University Press (OUP)

Subject

Cancer Research,General Medicine

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