Knockdown of CDCA5 suppresses malignant progression of breast cancer cells by regulating PDS5A

Abstract

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.

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

“…Furthermore, the knockdown of CDCA5 significantly inhibited cell growth and tumorigenesis in vitro and in vivo . Therefore, consistent with the findings of previous research ( 43 ), the results of the present study support an oncogenic role for CDCA5 in BC progression and suggest the possibility of the use of CDCA5 as a therapeutic target for breast cancer.…”

“…CDCA5 is aberrantly expressed in various types of cancer, such as hepatocellular carcinoma (35)(36)(37), bladder cancer (38), prostate cancer (39) and renal clear cell carcinoma (40), rendering it a potentially important prognostic marker and potential therapeutic target for cancer patients. However, only a limited number of studies (41)(42)(43) to date have investigated the expression and function of CDCA5 in BRCA.…”

Tubular IKKβ Deletion Alleviates Acute Ischemic Kidney Injury and Facilitates Tissue Regeneration

“…At 2 days after I/R injury, mRNA inducing cell proliferation, such as Azin1 [ 24 ], Depcd1a [ 25 ], Dsg2 [ 26 ], Gpr171 [ 27 ] and Kif18a [ 28 ], were lower in IKKβ ∆Tub compared to control, which is in line with the evaluation of Ki-67 positive cells at 2 days after I/R injury. This phenomenon is inversed at 14 days after I/R injury with higher proliferation rates in IKKβ ∆Tub compared to control and together with higher mRNA level of Tinagl1 [ 29 ] inducing cell proliferation and lower levels of Cdca5 [ 30 ] suspending cell proliferation. These time differences in cell proliferation are in line with transient cell cycle arrest, which was shown to be protective in acute kidney injury [ 31 ].…”