CDCA2 (Cell Division Cycle Associated 2)

The phosphorylation levels of protein kinase B (AKT) and mechanistic target of rapamycin (mTOR) were reduced by CDCA2 knockdown (P < 0.01), but the effect was reversed by the AKT activator SC-79 (P < 0.01). CDCA2 is a potential target to reverse cisplatin resistance in ovarian cancer. It can also be used as a new research direction for the development of ovarian cancer therapy.

Functional in vitro and in vivo studies revealed that knockout of CDCA2 decreased DLBCL cell proliferation and a bortezomib dose-response analysis showed less sensitivity in CDCA2 knockout cells compared to control cells. This study shows that DLBCL patients with high CDCA2 expression benefitted from the addition of bortezomib to R-CHOP and functional studies documented a direct impact of CDCA2 on the bortezomib response in DLBCL cells.

This study highlights CDCA genes as promising diagnostic and prognostic biomarkers in breast cancer. Their upregulation correlates with poor survival, and the knockdown of CDCA2 and CDCA3 impairs tumor growth, emphasizing their potential as therapeutic targets. These findings suggest that CDCA genes could be integrated into clinical practice for improved breast cancer management.

Therefore, CDCA2 holds great potential as both a biomarker for diagnosis and a therapeutic target for interventions such as targeted therapies or immunotherapy. Given its promising prospects in scientific research and clinical applications, it is imperative for researchers to delve into the underlying mechanisms of CDCA2 and explore its utilization.

In addition, CDCA2 knockout cells were also less sensitive to carfilzomib, a 2nd generation proteasome inhibitor. DLBCL patients with high expression levels of CDCA2 benefitted the most from addition of bortezomib to R-CHOP. In functional studies, the loss of CDCA2 increased cellular resistance to bortezomib in both single- and combinational drug studies.

CDCA2 can serve as a novel biomarker for the diagnosis and prognosis in pan-cancer, especially in LGG. For the development of novel targeted therapies in LGG, it may be a potential molecular target. However, to be sure, we'll need to do additional biological experiments to back up our results from bioinformatic predictions.

CDCA2, which was upregulated in melanoma, enhanced AURKA protein stability by inhibiting SMAD specific E3 ubiquitin protein ligase 1-mediated AURKA ubiquitination, thus playing a carcinogenic role in melanoma progression.