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A compelling relationship exists between high CDK2AP1 mRNA expression and lower TNM classification of breast cancer, which is consistent with CDK2AP1 having a tumour-suppressive function.
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Knockdown of CDK2AP1 in hESCs results in increased p53 and enhances differentiation and favors it over a self-renewal fate.
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DOC1 re-expression in oral cancer cells causes a reversal of EMT. DOC1 promotes NURD binding to a subset of target loci.
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The simultaneous overexpression of p12CDK2-AP1 and CD82 significantly suppressed the in vivo tumor growth.
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knockdown of CDK2AP1 in primary human fibroblasts reduced proliferation and induced premature senescence, with the observed phenotype being p53 dependent
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In summary, p12CDK2AP1 expression in myxofibrosarcoma cells induces G0/G1 arrest and mitochondria dependent proapoptotic activity and down-regulation of p12CDK2AP1 by shRNAi results in up-regulation of the CDK2 transcript and protein.
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Study reports that knockdown of CDK2AP1 by RNAi in glioma cells could effectively inhibit cell proliferation by inducing cell cycle arrest and apoptosis
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CDK2AP1 plays an important role in modulating the growth and tumorigenesis of lung cancer cells.
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Low CDK2AP1 expression is common and associated with adverse prognosis in nasopharyngeal carcinoma.
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Human cyclin-dependent kinase 2-associated protein 1 (CDK2AP1) is dimeric in its disulfide-reduced state, with natively disordered N-terminal region
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exerts its effect on stem cell maintenance/differentiation through epigenetic regulation [review]
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In comparison with the healthy gingiva, the expression of Doc-1 was decreased, whereas the expression of S100A7 was upregulated in all oral lesions.
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P12(CDK2AP1) is downregulated by miR-21
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Missing down-regulation of the tumor-suppressor gene DOC-1, might exert protective effects and counteract malignant transformation of benign, proliferating lesions of the oral cavity.
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Data support the role of cdk2ap1 as a tumor suppressor gene that can regulate squamous cell carcinoma growth in a cell autonomous manner through decreases in invasiveness and a non-cell autonomous manner through decreases in angiogenesis phenotypes.
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The combination of an increased expression of the antimicrobial peptide DEFA-4, the oncogene S100-A7, epidermal growth factor, and tenascin-c, and a decreased Doc-1 expression in oral leukoplakia might characterize its potency of malignant transformation.
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Results indicate that DOC-1 is a bona fide subunit of the Mi-2/NuRD chromatin remodeling complex.
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CDK2AP1 is a novel multiple sclerosis susceptibility loci, and it's risk allele correlates with diminished RNA expression of the cell cycle regulator CDK2AP1
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Data show low or moderate methylation was found in seven selected genes BAD, BBC3, CAV1, CDK2AP1, NPM1, PRKCDBP and THEM4.
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DOC1 has a differential expression in microsatellite-unstable human colorectal neoplasms.
