ArticleNeoplasia (New York, N.Y.)2021
CKB inhibits epithelial-mesenchymal transition and prostate cancer progression by sequestering and inhibiting AKT activation.
Article in Neoplasia (New York, N.Y.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
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- Single-cell and spatial transcriptomics reveal that the CXCL12-CXCR4 axis drives the immune-desert phenotype in small cell lung cancer by recruiting immunosuppressive CXCR4Journal for immunotherapy of cancer · 2026Article
- Mesenchymal to epithelial transition (MET) in cancer progression: insights from logical modeling.Scientific reports · 2026Article
- Cross-cohort multi-omics analysis identifies novel clusters driven by epithelial-mesenchymal transition signatures in gastric cancer.Cancer cell international · 2026Article
- Complement System-Related Genes in Diabetic Nephropathy: Screening for Potential Targets of the Mechanism.Journal of diabetes research · 2026Article
- Creatine kinase B, a downstream effector of c-Myb, controls migration of osteosarcoma cells via regulation of N-cadherin.Cancer cell international · 2025Article
- Creatine Kinase Blockade Disrupts Energy Metabolism and Redox Homeostasis to Suppress Osteosarcoma Progression.International journal of molecular sciences · 2025Article
- Prognostic model identification of ribosome biogenesis-related genes in pancreatic cancer based on multiple machine learning analyses.Discover oncology · 2025Article
- CKMT1B regulates the proliferation, migration, invasion, and apoptosis of colorectal cancer cells through the AKT/mTOR/STAT3 pathway.Molecular genetics and genomics : MGG · 2025Article
- Hormone correction of dysfunctional metabolic gene expression in stem cell-derived liver tissue.Stem cell research & therapy · 2025Article
- BAY11-7082 Targets RNF25 to Reverse TRIP4 Ubiquitination-dependent NF-κB Activation and Apoptosis Resistance in Renal Cell Carcinoma.International journal of biological sciences · 2025Article
- Targeting mRNA-coding genes in prostate cancer using CRISPR/Cas9 technology with a special focus on androgen receptor signaling.Cell communication and signaling : CCS · 2024Review
- Preoperative low plasma creatine kinase levels predict worse survival outcomes in bladder cancer after radical cystectomy.International urology and nephrology · 2024Article
- Androgen deprivation induces neuroendocrine phenotypes in prostate cancer cells through CREB1/EZH2-mediated downregulation of REST.Cell death discovery · 2024Article
- Androgen deprivation induces neuroendocrine phenotypes in prostate cancer cells through CREB1/EZH2-mediated downregulation of REST.Research square · 2023Article
- Targeting PI3K/Akt signaling in prostate cancer therapy.Journal of cell communication and signaling · 2023Review
- NSD3, a member of nuclear receptor-binding SET domain family, is a potential prognostic biomarker for pancreatic cancer.Cancer medicine · 2023Article
- LncRNA TYMSOS is a novel prognostic biomarker associated with immune infiltration in prostate cancer.American journal of cancer research · 2023Article
- New panel of biomarkers to discriminate between amelanotic and melanotic metastatic melanoma.Frontiers in oncology · 2022Article
- A Prognostic Survival Model of Pancreatic Adenocarcinoma Based on Metabolism-Related Gene Expression.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
18 authors at 9 institutions in 3 countries.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) contributes to tumor invasion, metastasis and drug resistance. AKT activation is key in a number of cellular processes. While many positive regulators for either EMT or AKT activation have been reported, few negative regulators are established. Through kinase cDNA screen, we identified brain-type creatine kinase (CKB or BCK) as a potent suppressor for both. As a ubiquitously expressed kinase in normal tissues, CKB is significantly downregulated in several solid cancer types. Lower CKB expression is significantly associated with worse prognosis. Phenotypically, CKB overexpression suppresses, while its silencing promotes, EMT and cell migration, xenograft tumor growth and metastasis of prostate cancer cells. AKT activation is one of the most prominent signaling events upon CKB silencing in prostate cancer cells, which is in line with prostate cancer TCGA data. EMT enhanced by CKB silencing is abolished by AKT inhibition. Mechanistically, CKB interacts with AKT and sequestrates it from activation by mTOR. We further elucidated that an 84aa fragment at C-terminus of CKB protein interacts with AKT's PH domain. Ectopic expression of the 84aa CKB fragment inhibits AKT activation, EMT and cell proliferation. Interestingly, molecular dynamics simulation on crystal structures of AKT and CKB independently demonstrates that AKT's PH domain and CKB's 84aa fragment establish their major interaction interface. In summary, we have discovered CKB as a negative regulator of EMT and AKT activation, revealing a new mode of their regulation . We have also demonstrated that CKB downregulation is a poor prognosticator, which is sufficient to promote prostate cancer progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.