KIF11 overexpression

Our study demonstrated that KIF11 was upregulated in EC and was strongly associated with a poor prognosis. Notably, we found that reduced KIF11 expression inhibited EC cell proliferation, migration and invasion. KIF11 knockdown caused more EC cells to arrest in the G2/M phase and undergo apoptosis. The findings of our study emphasized that KIF11 may be a promising prognostic biomarker and therapeutic target for EC patients.

Mechanistically, we revealed MG53's transcriptional control over KIF11, leading to cell cycle arrest. Our findings position MG53 as a promising tumor suppressor in PDAC, offering a novel avenue for therapeutic intervention by regulating KIF11 expression.

MAGs may serve as diagnostic markers and miRNA therapeutic targets for pancreatic cancer. Among the MAGs, KIF11, RCC1, ADCY, and SDK1 may be early diagnostic markers.

Besides, Akt/CREB pathway was blocked by HELLS silencing, which was restored by KIF11 overexpression. Collectively, HELLS knockdown blocked Akt/CREB pathway by downregulating KIF11 expression, thereby inhibiting LUAD cell proliferation, invasion, migration, and promoting apoptosis.

Preclinically, our results indicate feasibility of ispinesib treatment in MB, specifically aggressive Group 3 MB. Importantly, p53-mutant SHH MB represents a poor molecular-subtype candidate for ispinesib therapy.

Elevated expression of KIF11 predicts poor clinical outcome in ccRCC patients. Downregulation of KIF11 may provide a new therapeutic strategy for ccRCC.

The subcutaneous xenograft models indicated that targeting MVA biogenesis (atorvastatin) is effective to restrict the in vivo growth of KIF11 PDAC. Taken together, our study identified that KIF11 could activate the MVA cross talk to drive PDAC progression and inhibiting the KIF11/MVA axis provided a therapeutic vulnerability in the treatment of PDAC.

Overexpression of KIF11 in lung cancer had a correlation with advanced pathological grade, advanced T stage, and presence of lymph node metastasis, which predicted poor prognosis. In summary, the present study revealed that KIF11 might be a key gene in the tumorigenesis of BPDE-related lung cancer, raising the possibility of KIF11 as a target for BPDE-induced lung cancer prevention and therapy.

Finally, western blot analysis demonstrated that ASPM in combination with KIF11 promoted the malignant progression of HCC by regulating the activity of the Wnt/β-catenin signaling pathway. Therefore, the present study demonstrated that ASPM may interact with KIF11 in HCC cells to promote the malignant progression of HCC via the Wnt/β-catenin signaling pathway.