CCNA2 acts as a novel biomarker in regulating the growth and apoptosis of colorectal cancer
Authors Gan Y, Li Y, Li T, Shu G, Yin G
Received 11 June 2018
Accepted for publication 1 September 2018
Published 31 October 2018 Volume 2018:10 Pages 5113—5124
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr Antonella D'Anneo
Yaqi Gan,1,2,* Yimin Li,1,2,* Tong Li,1,2 Guang Shu,2 Gang Yin1,2
1Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan Province, China; 2Department of Pathology, School of Basic Medical Sciences, Central South University, Changsha, Hunan Province, China
*These authors contributed equally to this work
Objective: Colorectal cancer (CRC) is considered to be the most prevalent malignant tumors that contribute to high cancer-related mortality. However, the signaling pathways involved in CRC and CRC-driven genes are largely unknown. We seek to discover a novel biomarker in CRC.
Materials and methods: All clinical CRC samples (n=33) were from Xiangya Hospital. We first selected CCNA2 by integrated bioinformatics analysis of four GSE databases. Next, the expression of CCNA2 in tissues and cell lines was verified by quantitative real-time PCR. The effects of CCNA2 on cell growth, proliferation, cell cycle, and apoptosis were examined by in vitro assays.
Results: We identified 498 shared DEGs (294 upregulated and 204 downregulated), and the top ten hub genes were selected by integrated analysis. These hub genes were significantly overexpressed in CRC samples and were positively correlated. Our data revealed that the expression of CCNA2 in CRC tissues is higher than that in normal tissues. The CCNA2 knockdown could significantly suppress CRC cell growth by impairing cell cycle progression and inducing cell apoptosis.
Conclusion: CCNA2, as a novel oncogenic gene, plays a role in regulating cancer cell growth and apoptosis. It could be used as a new biomarker for diagnosis and therapy in CRC.
Keywords: CCNA2, colorectal cancer, bioinformatics analysis, proliferation, cell cycle, apoptosis
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