CENPM (Centromere Protein M)

Cutaneous melanoma cell lines (A375 and SK-MEL-28) were transfected by CENPM siRNA (si-CENPM), followed by detections and treatment of various concentrations of dabrafenib and vemurafenib. Clinically, GEPIA database revealed that CENPM was upregulated and correlated with worse overall survival in cutaneous melanoma patients. Targeting CENPM suppresses cutaneous melanoma growth and mobility by inactivating AKT pathway, indicating its potential as a treatment target.

In vivo experiments confirmed that knocking down CENPM leads to reduced tumor growth in glioma models and improves the prognosis of tumor-bearing mice. This study underscores the critical role of CENPM in glioma and sheds light on potential therapeutic strategies.

CENPM is an independent prognostic factor for COAD, with its overexpression associated with improved survival. It regulates the cell cycle and tumor microenvironment, making it a promising potential predictive biomarker for immune therapy response.

TIDE analysis suggested that patients in the low-risk group may exhibit greater sensitivity to immune checkpoint inhibitor therapy. In conclusion, RRM2 and GAPDH represent promising prognostic and immunotherapeutic biomarkers, offering new avenues for LUAD treatment strategies.

Inhibition of either Wnt signaling or the CDC20/MYBL2 axis attenuated the tumorigenic potential and proliferative effects induced by CENPM. Our findings underscore the critical role of CENPM in driving NSCLC development and suggest that CENPM could serve as a novel biomarker for predicting NSCLC progression in clinical settings.

CENPM is the key gene that drives ACC metastasis, and a robust biomarker for ACC prognosis. Silencing CENPM impedes ACC metastasis in vitro and in vivo by physical interaction with immune checkpoint ligand FGL1. FGL1 is overexpressed in ACC and promotes ACC metastasis.

These findings underscore the E2F1-CENPM axis as a promising target for therapeutic strategies, aiming to disrupt the metabolic and invasive pathways facilitated by CENPM in GBM. These insights establish a foundation for targeting the metabolic dependencies of tumor cells, potentially leading to innovative treatments for GBM.

In summary, our study findings indicate that CENPM may serve as a cancer-causing gene in breast cancer and also as a biomarker for predicting the efficacy of immunotherapy. The oncogene CENPM is associated with breast cancer and is involved in cell proliferation and immune infiltration.

The upregulation of CENPM in ccRCC predicts a poor clinical outcome, and this malignant phenotype may be associated with its exacerbation of the immunosuppressive state in the tumor microenvironment.