CDCA5 promotes the progression of breast cancer and serves as a potential prognostic biomarker.

Oncol Rep

College of Life and Health Sciences, Institute of Biology and Medicine, Wuhan University of Science and Technology, Wuhan, Hubei 430000, P.R. China.

Published: October 2022

AI Article Synopsis

  • CDCA5 is highly expressed in breast cancer (BC) and its high levels are linked to poorer survival rates in patients.
  • Knockdown of CDCA5 in BC cell lines reduced cell proliferation, migration, and the ability to form colonies, indicating its role in cancer progression.
  • The study suggests that CDCA5 could serve as a useful biomarker for prognosis and a potential target for breast cancer therapy.

Article Abstract

Cell division cycle‑associated 5 (CDCA5) plays a critical role in the progression of various human cancers by regulating cell cycle‑related proteins; however, the function of CDCA5 in breast cancer (BC) is poorly understood. The aim of the present study was to investigate the expression level of CDCA5 in BC and its effect on BC progression. CDCA5 was found to be highly expressed in patients with BC, as well as in BC cell lines. It was also found that a high CDCA5 expression in BC was significantly associated with a shorter survival rate. In addition, the expression level of CDCA5 was significantly increased in stem cells derived from suspension‑cultured BC cells, as compared to adherent‑cultured cells. CDCA5 knockdown in MCF7 and SKBR3 cells significantly reduced cell proliferation, migration and clone formation. At the same time, the stemness capacity of BC cells, determined by analyzing cancer stem cell marker expression and mammosphere formation, was also markedly diminished following the knockdown of CDCA5. In addition, in vivo experiments demonstrated that CDCA5 knockdown in MCF7 cells markedly reduced tumor growth. On the whole, the present study demonstrates that CDCA5 may be used as a prognostic biomarker and therapeutic target for BC.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9478967PMC
http://dx.doi.org/10.3892/or.2022.8387DOI Listing

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