CDCA2 promotes breast cancer progression by downregulating KISS1 expression.

Breast cancer is a females' prevalent malignancy, resulting in higher mortality rates than other cancers. Therefore, exploring effective therapeutic targets and diagnostic biomarkers is critical for improving drugs' curative effect in treating breast cancer patients. The MDA-MB-231 and Michigan Cancer Foundation-7 (MCF-7) cells were transfected by pc-CDCA2, Small interfering RNA Negative Control (siNC), siCDCA2, and pc-KISS1 to investigate the effects of cell division cycle associated 2 (CDCA2) and kisspeptin 1 (KISS1) protein on breast cancer cell's viability, migration and invasion. Reverse Transcription Quantitative Polymerase Chain Reaction (RT-qPCR) was used to examine the CDCA2 mRNA expression. Impact of CDCA2 and KISS1 on invasion ability, motility and viability of breast cancer cells were detected via colony-forming unit, Cell Counting Kit-8 (CCK-8) and transwell assay. The Annexin V-Fluorescein Isothiocyanate (annexin V-FITC) staining was employed to determine the cellular apoptosis ratio based on flow cytometry. Findings indicated that CDCA2 expression got increased in breast cancer tissues, which greatly enhanced the cell proliferation, migration and invasion ability. Moreover, the regulation of CDCA2 may suppress the activation of KISS1 in breast cancer cells. In summary, the findings depicted that in breast cancer cells, the CDCA2 expression was enhanced to promote cells motility, invasiveness and viability through inhibition of KISS1 expression. Therefore, targeted gene therapy to suppress the expression levels of CDCA2 and upregulation of the KISS1 have the potential to be promising therapeutic strategies for treating breast cancer metastasis. [ABSTRACT FROM AUTHOR]