ArticleBMC cancer2015
Critical role of CDK11(p58) in human breast cancer growth and angiogenesis.
Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- Histone acetyltransferase HBO1 in cancer biology: Essential mechanisms and implications for targeted therapeutics.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- Targeting Transcriptional Cyclin-Dependent Kinases in Cancer.Molecular cancer therapeutics · 2025Review
- Mechanistic Roles of Transcriptional Cyclin-Dependent Kinases in Oncogenesis: Implications for Cancer Therapy.Cancers · 2025Review
- Cyclin-dependent protein kinases and cell cycle regulation in biology and disease.Signal transduction and targeted therapy · 2025Review
- The Roles of Cyclin-Dependent Kinases in Cell-Cycle Progression and Therapeutic Strategies in Human Breast Cancer.International journal of molecular sciences · 2020Review
- miR106a Promotes the Growth of Transplanted Breast Cancer and Decreases the Sensitivity of Transplanted Tumors to Cisplatin.Cancer management and research · 2020Article
- CDK11Cell cycle (Georgetown, Tex.) · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA capillary network is needed in cancer growth and metastasis. Induction of angiogenesis represents one of the major hallmarks of cancer. CDK11(p58), a Ser/Thr kinase that belongs to the Cell Division Cycle 2-like 1 (CDC2L1) subfamily is associated with cell cycle progression, tumorigenesis, sister chromatid cohesion and apoptotic signaling. However, its role in breast cancer proliferation and angiogenesis remains unclear.
methodsTumorigenicity assays and blood vessel assessment in athymic mice were used to assess the function of CDK11(p58) in tumor proliferation and angiogenesis. CCK-8 assay was used to detect breast cancer cell growth. Immunohistochemistry was used to detect the expression of vascular endothelial growth factor (VEGF), CD31 and CD34 in CDK11 positive patient breast cancer tissues. Dual-Luciferase array was used to analyze the function of CDK11(p58) in the regulation of VEGF promoter activity. Western blot was used to detect related protein expression levels.
resultsCDK11(p58) inhibited breast cancer growth and angiogenesis in breast cancer cells and in nude mice transplanted with tumors. Immunohistochemistry confirmed that CDK11(p58) was negatively associated with angiogenesis-related proteins such as VEGF, CD31 and CD34 in breast cancer patients. Real-time PCR and dual-luciferase assay showed CDK11(p58) inhibited the mRNA levels of VEGF and the promoter activity of VEGF. As CDK11(p58) is a Ser/Thr kinase, the kinase-dead mutant failed to inhibit VEGF mRNA and promoter activity. Western blot analysis showed the same pattern of related protein expression. The data suggested angiogenesis inhibition was dependent on CDK11(p58) kinase activity.
conclusionThis study indicates that CDK11(p58) inhibits the growth and angiogenesis of breast cancer dependent on its kinase activity.
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