ArticleCancer medicine2022
KIF11 manipulates SREBP2-dependent mevalonate cross talk to promote tumor progression in pancreatic ductal adenocarcinoma.
Article in Cancer medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- The antitumoral effect of statins in pancreatic ductal adenocarcinoma: a scoping review.Frontiers in pharmacology · 2026Pooled it
- Molecular Dynamics Simulations Provide Further Insights into the Allosteric Regulation of the Kinesin-5 Motor Domain by Loop 5.Journal of chemical information and modeling · 2026Article
- Mevalonate pathway in pancreatic ductal adenocarcinoma: Mechanisms driving metabolic and cellular plasticity.Cancer pathogenesis and therapy · 2026Review
- Kinesin Spindle Protein (KIF11) in Mitosis and Cancer.International journal of molecular sciences · 2025Review
- Long-Term Dietary Consumption of Grapes Alters Phenotypic Expression in Skeletal Muscle of Aged Male and Female Mice.Foods (Basel, Switzerland) · 2025Article
- miR-584-5p Regulates MSMO1 to Modulate the AKT/PI3K Pathway and Inhibit Breast Cancer Progression.Protein and peptide letters · 2025Article
- SREBP2 as a central player in cancer progression: potential for targeted therapeutics.Frontiers in pharmacology · 2025Review
- Mechanisms ofAmerican journal of translational research · 2025Article
- A novel tumor-derived exosomal gene signature predicts prognosis in patients with pancreatic cancer.Translational cancer research · 2024Article
- PRMT1 promotes epigenetic reprogramming associated with acquired chemoresistance in pancreatic cancer.Cell reports · 2024Article
- SKA3 Expression as a Prognostic Factor for Patients with Pancreatic Adenocarcinoma.International journal of molecular sciences · 2024Article
- Mitotic Functions and Characters of KIF11 in Cancers.Biomolecules · 2024Review
- Eg5 and Diseases: From the Well-Known Role in Cancer to the Less-Known Activity in Noncancerous Pathological Conditions.Biochemistry research international · 2024Review
- KIF11 promotes vascular smooth muscle cell proliferation by regulating cell cycle progression and accelerates neointimal formation after arterial injury in mice.Frontiers in pharmacology · 2024Article
- Cholesterol metabolism in tumor microenvironment: cancer hallmarks and therapeutic opportunities.International journal of biological sciences · 2024Review
- Identification of Promising Drug Candidates against Prostate Cancer through Computationally-Driven Drug Repurposing.International journal of molecular sciences · 2023Article
- Integrated analysis ofFrontiers in pharmacology · 2023Article
- KIF11 manipulates SREBP2-dependent mevalonate cross talk to promote tumor progression in pancreatic ductal adenocarcinoma.Cancer medicine · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cholesterol metabolism is highly correlated with risks of pancreatic ductal adenocarcinoma (PDAC). Nevertheless, the underlying mechanisms of activation of cholesterol biogenesis remain inconclusive. KIF11 is a key component of the bipolar spindle and expresses highly in various malignancies. However, its functional role in PDAC tumorigenesis is still unclear. This study aims to elucidate the oncogenic functions of KIF11 in stimulating cholesterol metabolism, thereby driving PDAC progression. We utilized bioinformatics analysis to identify that KIF11 expressed highly in tumor samples versus paired normal tissues and high KIF11 correlated with high clinical stages of patients. Patients with high KIF11 had worse survival outcomes relative to those with low KIF11. Gene set enrichment analysis (GSEA) revealed that KIF11 correlated intensively with the mevalonate (MVA) metabolic pathway. Positive associations were observed between KIF11 and MVA-signature (HMGCR, FDFT1, SQLE, and MSMO1). KIF11 could elevate the free cholesterol content of PDAC cells and targeting MVA inhibited the in vitro growth of KIF11-overexpressing cells. Mechanistically, we found KIF11 could interact with SREBP2, the master regulator of MVA. High KIF11 could increase SREBP2 proteins, but not alter their mRNA levels. KIF11 could attenuate the ubiquitination-mediated degradation of SREBP2, thereby enhancing its stability and accumulation. Accordingly, KIF11 stimulated the expressions of MVA-signature and free cholesterol contents depending on SREBP2. In addition, KIF11 depended on SREBP2 to promote cell growth, migration, stemness, and colony formation abilities. The subcutaneous xenograft models indicated that targeting MVA biogenesis (atorvastatin) is effective to restrict the in vivo growth of KIF11
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