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These results suggest that miR-125a-3p can function as a novel tumor suppressor in ER(+) breast cancer by targeting CDK3, which may be a potential therapeutic approach for TamR breast cancer therapy
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HuR facilitated lung cancer stemness dependent on CDK3 expression. miR-873 or miR-125a-3p level was negatively correlated with HuR and CDK3 expression levels in lung cancer tissues. HuR facilitates lung cancer stemness via regulating miR-873/CDK3 and miR-125a-3p/CDK3 axis.
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ectopic expression of HuR promotes breast cancer cell proliferation and survival by directly binding to and stabilizing CDK3 mRNA.
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These results provided evidence supporting the oncogenic potential of NFAT3 and suggested that CDK3-mediated phosphorylation of NFAT3 has an important role in skin tumorigenesis.
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The analysis of tumor and matched normal lung tissues indicates that miR-150 downregulation in lung tumors correlates with higher CDK3 levels. In addition, miR-150 transfection experiments with cancer-derived cell lines reveal that miR-150-mediated CDK3 suppression directly induces growth inhibition.
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High Cdk3-promoted epithelial-mesenchymal transition through activating AP-1 is involved in colorectal cancer metastasis.
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Data indicate that microRNA miR-214 has tumor-suppressive activity in hepatocellular carcinoma (HCC) through inhibition of E2F2 transcription factor (E2F2), cyclin-dependent kinases CDK3 and CDK6.
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Mir-873 inhibits ESR1 activity and cell growth via targeting CDK3.
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CDK3 is associated with the progression of NPC, and may be a potential biomarker for prediction of the prognosis of patients with NPC.
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The Walleye dermal sarcoma virus cyclin functions as a structural ortholog of cyclin C in spite of its limited amino acid sequence identity with C cyclins or with any known cyclins and activates Cdk8 and Cdk3.
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A non-cdk8-associated cellular pool of cyclin C combines with cdk3 to stimulate pRb phosphorylation at S807/811 during the G0/G1 transition, and this phosphorylation is required for cells to exit G0 efficiently.
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Expression level of cdk3 is higher in human cancer cell lines and glioblastoma tissue compared with normal brain tissue. cdk3 phosphorylates activating transcription factor 1 (ATF1)and enhances the transactivation and transcriptional activities of ATF1.