S100 Calcium Binding Protein A10, A Novel Oncogene, Promotes the Proliferation, Invasion, and Migration of Hepatocellular Carcinoma

Xing Zhou; Min Shi; Jun Cao; Tianwen Yuan; Guanzhen Yu; Ying Chen; Wenzheng Fang; Hongwei Li

doi:10.3389/fgene.2021.695036

S100 Calcium Binding Protein A10, A Novel Oncogene, Promotes the Proliferation, Invasion, and Migration of Hepatocellular Carcinoma

Front Genet. 2021 Jun 11:12:695036. doi: 10.3389/fgene.2021.695036. eCollection 2021.

Authors

Xing Zhou¹, Min Shi², Jun Cao¹, Tianwen Yuan¹, Guanzhen Yu^{3

4}, Ying Chen⁵, Wenzheng Fang⁶, Hongwei Li³

Affiliations

¹ Department of Interventional Oncology, Dahua Hospital, Shanghai, China.
² Department of Pathology, Sichuan Cancer Center, School of Medicine, Sichuan Cancer Hospital & Institute, University of Electronic Science and Technology of China, Chengdu, China.
³ Department of Oncology, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.
⁴ Shanghai Key Laboratory of Multidimensional Information Processing, East China Normal University, Shanghai, China.
⁵ Department of Gastroenterology, Naval Medical University, Shanghai, China.
⁶ Department of Oncology, Clinical Medical College of Fujian Medical University (900 Hospital of the Joint Logistics Team), Fujian, China.

Abstract

Hepatocarcinogenesis is a highly complicated process that is promoted by a series of oncogenes. Our study aims to identify novel oncogenes promoting hepatocellular carcinoma (HCC) by bioinformatic analysis and experimental validation. Here, we reported that S100 calcium binding protein A10 (S100A10) was screened out as a potential novel oncogene in HCC by integrated analysis of OEP000321 dataset and the Cancer Genome Atlas (TCGA)-Liver-Cancer data. Furthermore, S100A10 was highly expressed in HCC samples and observably associated with patients' overall survival (OS). Overexpression of S100A10 in Hep3B and Huh-7 increased the cell proliferation, whereas downregulation of S100A10 in SK-Hep-1 and HepG2 cells reduced the cell viability to almost stop growing. In vivo tumor growth assays showed that S100A10-overexpressing Hep3B cells had a larger tumor size than control. Moreover, S100A10 overexpression promoted Hep3B cells migration and invasion, and S100A10 knockdown inhibited SK-Hep-1 cells migration and invasion, in vitro. In conclusion, it is demonstrated that S100A10 is a novel oncogene in HCC, indicating a possible novel therapeutic strategy of HCC.

Keywords: S100A10; hepatocellular carcinoma; in vivo; invasion; migration; proliferation.