Open AccessKnockdown of CDCA5 suppresses malignant progression of breast cancer cells by regulating PDS5A
Author(s) -
Yan Wang,
Jing Yao,
YongGuan Zhu,
Xiuchen Zhao,
Jing Lv,
Fulan Sun
Publication year - 2022
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2022.12725
Subject(s) - cell cycle , cancer research , gene knockdown , cell growth , biology , oncogene , breast cancer , cancer , small hairpin rna , cancer cell , cell migration , cell , cell culture , genetics
Breast cancer is one of the most common malignant tumors in women. Cell division cycle‑associated 5 (CDCA5) is closely associated with the behavior of various cancer types. The aim of the present study was to explore the effect of CDCA5 on breast cancer. Western blot analysis and reverse transcription‑quantitative PCR were used to detect the expression level of CDCA5 in human normal mammary cells and human breast cancer cell lines. To determine its function in MDA‑MB‑231 cells, CDCA5 was silenced in MDA‑MB‑231 cells by transient short hairpin RNA transfection. Cell Counting Kit‑8 and clonogenicity assays were used to evaluate cell proliferation. Wound healing and Transwell assays were used to detect cell invasion and migration. Western blot analysis was used to detect the protein expressions of Ki67 and PCNA associated with proliferation, MMP2 and MMP9 associated with migration. CDCA5 was found to be markedly increased in breast cancer cell lines. CDCA5 knockdown was able to suppress cell proliferation, invasion and migration. CDCA5 inhibition downregulated PDS5 cohesin‑associated factor A (PDS5A) expression in breast cancer cells. PDS5A overexpression was found to reverse the effect of CDCA5 inhibition on breast cancer cell proliferation and migration. CDCA5 knockdown was shown to suppress the malignant progression of breast cancer cells by regulating PDS5A. The present findings may provide new potential targets for breast cancer therapy.