CDCA2 Inhibits Apoptosis and Promotes Cell Proliferation in Prostate Cancer and Is Directly Regulated by HIF-1α Pathway.

CDCA2 HIF-1a apoptosis proliferation prostate cancer

Journal

Frontiers in oncology
ISSN: 2234-943X
Titre abrégé: Front Oncol
Pays: Switzerland
ID NLM: 101568867

Informations de publication

Date de publication:
2020
Historique:
received: 18 11 2019
accepted: 16 04 2020
entrez: 9 6 2020
pubmed: 9 6 2020
medline: 9 6 2020
Statut: epublish

Résumé

Prostate cancer (PCa) is a major serious malignant tumor and is commonly diagnosed in older men. Identification of novel cancer-related genes in PCa is important for understanding its tumorigenesis mechanism and developing new therapies against PCa. Here, we used RNA sequencing to identify the specific genes, which are upregulated in PCa cell lines and tissues. The cell division cycle associated protein (CDCA) family, which plays a critical role in cell division and proliferation, is upregulated in the PCa cell lines of our RNA-Sequencing data. Moreover, we found that

Identifiants

pubmed: 32509575
doi: 10.3389/fonc.2020.00725
pmc: PMC7248370
doi:

Types de publication

Journal Article

Langues

eng

Pagination

725

Informations de copyright

Copyright © 2020 Zhang, Cheng, Zhang, Bai, Jin, Guo, Huang, Li, Wang, Shu, Yuan and Ying.

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Auteurs

Yixiang Zhang (Y)

Department of Urology, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.

Yingduan Cheng (Y)

Department of Translational Molecular Medicine, Saint John's Health Center, John Wayne Cancer Institute, PHS, Santa Monica, CA, United States.

Zhaoxia Zhang (Z)

Department of Pediatrics, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.

Zhongyuan Bai (Z)

Department of Urology, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.

Hongtao Jin (H)

Department of Pathology, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.

Xiaojing Guo (X)

Department of Pathology, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.

Xiaoyan Huang (X)

Department of Physiology, School of Basic Medical Sciences, Shenzhen University Health Sciences Center, Shenzhen University, Shenzhen, China.

Meiqi Li (M)

Department of Physiology, School of Basic Medical Sciences, Shenzhen University Health Sciences Center, Shenzhen University, Shenzhen, China.

Maolin Wang (M)

Department of Physiology, School of Basic Medical Sciences, Shenzhen University Health Sciences Center, Shenzhen University, Shenzhen, China.

Xing-Sheng Shu (XS)

Department of Physiology, School of Basic Medical Sciences, Shenzhen University Health Sciences Center, Shenzhen University, Shenzhen, China.

Yeqing Yuan (Y)

Department of Urology, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.

Ying Ying (Y)

Department of Physiology, School of Basic Medical Sciences, Shenzhen University Health Sciences Center, Shenzhen University, Shenzhen, China.

Classifications MeSH