Cyclin-dependent kinases regulatory subunit 1 (CKS1B)

Cyclin-dependent kinases regulatory subunit 1 (CKS1B) is a highly conserved regulatory protein that binds cyclin-dependent kinases (CDKs), facilitating their activity in cell cycle progression[1][2][4]. CKS1B plays an essential role in cell division, specifically enabling the transition from G1 to S phase by promoting the ubiquitin-mediated degradation of CDK inhibitors like p27^Kip1 and p21^Cip1 through interaction with the SCF-Skp2 complex[1][2]. Overexpression of CKS1B drives tumor proliferation, metastasis, and chemoresistance in multiple malignancies, while its depletion causes mitotic arrest and impairs cancer growth[2][3]. High CKS1B expression is linked to poor prognosis—particularly in multiple myeloma and several solid tumors—and promotes resistance to chemotherapy by activating oncogenic pathways, such as MEK/ERK and STAT3, and by enhancing heat shock protein 90 (Hsp90) activity[2]. Although CKS1B is not yet directly druggable in the clinic, it represents an emerging precision oncology target and prognostic biomarker for several aggressive cancers[2][3].

Other names

CKS1PNAS-16PNAS-18CKS-1CDC28 protein kinase regulatory subunit 1Bckshs1CDC2-associated protein CKS1NB4 apoptosis/differentiation related proteincell division control protein CKS1

Inhibition of CKS1B may reverse drug resistance and sensitize tumor cells to chemotherapy (e.g., bortezomib, cisplatin, doxorubicin) by restoring degradation of CDK inhibitors and blocking MEK/ERK and STAT3 pathways[2].