NEK6 (NIMA Related Kinase 6)

NEK6 may function as a prognostic and immune-regulatory biomarker in ccRCC. Coriander flavonoids could target NEK6 to modulate the immune microenvironment, providing new insight into plant-based therapeutic strategies for ccRCC.

Our results disclosed that NEK6 heightened HCC progression and glycolysis through ubiquitination of TCP10L. Our study may provide a new perspective for the treatment of HCC.

NEK6 is highly expressed in OC; its overexpression indicates poor prognosis; and NEK6 knockdown leads to inhibited growth, migration and invasion while promoting the apoptosis of OC cells. These findings indicate that NEK6 is a potential oncogene and a poor prognostic factor in OC, suggesting that NEK6 can serve as a new therapeutic candidate for OC and that NEK6 inhibition may be an effective strategy for OC treatment.

The expression level of cNEK6 in the peripheral blood and tumor tissues correlated significantly and positively with the activation of the mTORC1 pathway and degree of glycolysis. Hence, the therapeutic effect of gemcitabine is limited in patients with high cNEK6 levels, and in combination with the mTORC1 inhibitor, rapamycin, can enhance sensitivity to gemcitabine chemotherapy.

The NEK6-mediated reprogramming of de novo purine synthesis emerges as a critical pathway influencing chemoresistance in ovarian cancer. Paeonol exhibits the potential to interfere with NEK6, thereby inhibiting chemoresistance.

The simulations revealed that the R171Q variant was unstable and led to significant conformational changes in NEK6. This study provides valuable insights into NEK6 dysfunction caused by single amino acid alterations, offering a novel understanding of the molecular mechanisms underlying NEK6-related cancer progression.

CircNEK6 serves as a competing endogenous RNA of CCND1 by absorbing miR-503, which might be treated as a novel and potential target for PDAC treatment.

NEK6 can promote osteosarcoma progression via activating STAT3 signaling pathway, which is inhibited by miR-26a-5p, suggesting that NEK6 is a potential oncogene and miR-26a-5p is a suppressor of osteosarcoma. The strategy of inhibiting of NEK6 by miR-26a-5p may be an effective approach for osteosarcoma therapy.