ArticleCancer medicine2023
Cyclin-dependent kinase subunit2 (CKS2) promotes malignant phenotypes and epithelial-mesenchymal transition-like process in glioma by activating TGFβ/SMAD signaling.
Article in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Prognostic significance of cyclin-dependent kinase subunit 2 (CKS2) in malignant tumours: a meta-analysis and bioinformatic analysis.BMJ open · 2024Pooled it
- DNMT1 blocks SOX21-repressed CKS2 transcription to promote gastric cancer progression.BMC cancer · 2025Article
- Diamond Nanoparticles Suppress Migration of T98G Glioblastoma Cells by Targeting ECM-Integrin Interactions and Intracellular Signaling, Leading to Extensive Proteome Alterations.Nanotechnology, science and applications · 2025Article
- CKS2 Silencing Affects Proliferation and Apoptosis in Multiple Myeloma through the PTEN/ AKT/mTOR Pathway.Journal of Cancer · 2025Article
- CKS2 induces autophagy-mediated glutathione metabolic reprogramming to facilitate ferroptosis resistance in colon cancer.Molecular medicine (Cambridge, Mass.) · 2024Article
- Integrated analysis of histone modification features in clear cell renal cancer for risk stratification and therapeutic prediction.Translational oncology · 2024Article
- Identification of copper death-associated molecular clusters and immunological profiles for lumbar disc herniation based on the machine learning.Scientific reports · 2024Article
- Molecular and clinical characterization of atypical central neurocytomas: implications for diagnosis and treatment strategies.Discover oncology · 2024Article
- Biological functions and therapeutic potential of CKS2 in human cancer.Frontiers in oncology · 2024Review
- Review
- Cyclin-dependent kinase subunit2 (CKS2) promotes malignant phenotypes and epithelial-mesenchymal transition-like process in glioma by activating TGFβ/SMAD signaling.Cancer medicine · 2023Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGliomas are a group of primary intracranial tumors with high morbidity and mortality. The previous researches indicated a crucial role of CKS2 (cyclin-dependent kinases regulatory subunit 2) in hepatocellular carcinoma and breast cancer; however, little is known about the molecular mechanism of CKS2 in the tumorigenesis and epithelial-mesenchymal transition-like (EMT) process in glioma.
methodsDatasets for bioinformatics analysis were obtained from the GEO, TCGA and CGGA databases. qRT-PCR, western blotting (WB), and immunohistochemistry (IHC) assays were used to investigate the expression patterns of CKS2 among glioma and brain tissues. Glioma cells were transfected with small interfering RNA/overexpression plasmid against CKS2, then clone formation assay, CCK-8, wound healing, Transwell assay, and flow cytometry were performed to detect changes in cell viability, invasiveness, and the apoptosis rate. Markers of cell invasion, apoptosis, EMT and TGFβ/SMAD signaling were evaluated by WB and immunofluorescence (IF) assays.
resultsWe found that CKS2 overexpression correlates with poor prognosis in human glioma and knockdown of CKS2 could inhibit cell proliferation, migration, invasion, and induced apoptosis in glioma cells. Besides, we also found that knockdown of CKS2 could reverse the EMT process via modulating EMT-related molecules. Glioma cells with overexpression of CKS2 were constructed to confirmed the fact that CKS2 induced nucleocytoplasmic translocation of SMAD2/3 and activated TGFβ/SMAD pathway, then upregulated its downstream targets expression, while inhibition of TGFβ/SMAD (by TGFβ inhibitor LY2157299 or SMAD4 siRNA) could reverse the tumor-promoting effects and malignant phenotype caused by CKS2 overexpression.
conclusionsWe identified CKS2 as a critical contributor to the gliomagenesis, which might provide a novel therapeutic target for inhibiting the spread and infiltration of glioma.
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