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

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)...

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Main Authors: Xing Zhou, Min Shi, Jun Cao, Tianwen Yuan, Guanzhen Yu, Ying Chen, Wenzheng Fang, Hongwei Li
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-06-01
Series:Frontiers in Genetics
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fgene.2021.695036/full
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author Xing Zhou
Min Shi
Jun Cao
Tianwen Yuan
Guanzhen Yu
Guanzhen Yu
Ying Chen
Wenzheng Fang
Hongwei Li
author_facet Xing Zhou
Min Shi
Jun Cao
Tianwen Yuan
Guanzhen Yu
Guanzhen Yu
Ying Chen
Wenzheng Fang
Hongwei Li
author_sort Xing Zhou
collection DOAJ
description 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.
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spelling doaj.art-63f687c9a791483d9a3a8e85019bbbce2022-12-21T21:25:36ZengFrontiers Media S.A.Frontiers in Genetics1664-80212021-06-011210.3389/fgene.2021.695036695036S100 Calcium Binding Protein A10, A Novel Oncogene, Promotes the Proliferation, Invasion, and Migration of Hepatocellular CarcinomaXing Zhou0Min Shi1Jun Cao2Tianwen Yuan3Guanzhen Yu4Guanzhen Yu5Ying Chen6Wenzheng Fang7Hongwei Li8Department of Interventional Oncology, Dahua Hospital, Shanghai, ChinaDepartment of Pathology, Sichuan Cancer Center, School of Medicine, Sichuan Cancer Hospital & Institute, University of Electronic Science and Technology of China, Chengdu, ChinaDepartment of Interventional Oncology, Dahua Hospital, Shanghai, ChinaDepartment of Interventional Oncology, Dahua Hospital, Shanghai, ChinaDepartment of Oncology, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaShanghai Key Laboratory of Multidimensional Information Processing, East China Normal University, Shanghai, ChinaDepartment of Gastroenterology, Naval Medical University, Shanghai, ChinaDepartment of Oncology, Clinical Medical College of Fujian Medical University (900 Hospital of the Joint Logistics Team), Fujian, ChinaDepartment of Oncology, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaHepatocarcinogenesis 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.https://www.frontiersin.org/articles/10.3389/fgene.2021.695036/fullS100A10proliferationinvasionmigrationhepatocellular carcinomain vivo
spellingShingle Xing Zhou
Min Shi
Jun Cao
Tianwen Yuan
Guanzhen Yu
Guanzhen Yu
Ying Chen
Wenzheng Fang
Hongwei Li
S100 Calcium Binding Protein A10, A Novel Oncogene, Promotes the Proliferation, Invasion, and Migration of Hepatocellular Carcinoma
Frontiers in Genetics
S100A10
proliferation
invasion
migration
hepatocellular carcinoma
in vivo
title S100 Calcium Binding Protein A10, A Novel Oncogene, Promotes the Proliferation, Invasion, and Migration of Hepatocellular Carcinoma
title_full S100 Calcium Binding Protein A10, A Novel Oncogene, Promotes the Proliferation, Invasion, and Migration of Hepatocellular Carcinoma
title_fullStr S100 Calcium Binding Protein A10, A Novel Oncogene, Promotes the Proliferation, Invasion, and Migration of Hepatocellular Carcinoma
title_full_unstemmed S100 Calcium Binding Protein A10, A Novel Oncogene, Promotes the Proliferation, Invasion, and Migration of Hepatocellular Carcinoma
title_short S100 Calcium Binding Protein A10, A Novel Oncogene, Promotes the Proliferation, Invasion, and Migration of Hepatocellular Carcinoma
title_sort s100 calcium binding protein a10 a novel oncogene promotes the proliferation invasion and migration of hepatocellular carcinoma
topic S100A10
proliferation
invasion
migration
hepatocellular carcinoma
in vivo
url https://www.frontiersin.org/articles/10.3389/fgene.2021.695036/full
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