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CDK14 was validated to be the target protein the miR-139.
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OIP5-AS1 acts as a miR-223 'sponge' to trigger CDK14 expression to promote osteosarcoma tumorigenesis.
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knockdown of E2F5 and PFTK1 mimicked the tumor-suppressive effects of miR-1-3p overexpression on PCa progression. Conversely, concomitant knockdown of miR-1-3p and E2F5 and PFTK1 substantially reversed the inhibitory effects of either E2F5 or PFTK1 silencing alone.
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MiR-613 and CDK14 may serve as potential therapeutic targets for the treatment of glioma.
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CDK14 mediated miR-1202 to exert its anti-tumor effects.
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CDK14 expression was closely associated with poor prognosis and overall survival of Osteosarcoma patients. miR-216a inhibits CDK14 expression by binding to the 3'-untranslated region of CDK14.
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PFTK1 expression is significantly higher in CRC tissues compared with matched adjacent noncancerous colorectal tissues. The associations between PFTK1 expression and clinicopathological characters, and PFTK1 expression and the OS rate following resection suggested that PFTK1 may represent a novel biomarker of poor prognosis in CRC
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Results show that CDK14 and DYRK2 expression were inversely correlated in human breast cancer tissues and identified CDK14 as a target of DYRK2.
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miR-455 inhibits breast cancer cell proliferation through targeting CDK14
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findings revealed an unrecognized role of Caprin-2 in facilitating LRP5/6 constitutive phosphorylation at G2/M through forming a quaternary complex with CDK14, Cyclin Y, and LRP5/6.
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these results suggest that knockdown of PFTK1 inhibited the proliferation and invasion of colon cancer cells as well as the EMT progress by suppressing the Sonic hedgehog signaling pathway.
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we report that PFTK1 downregulation might inhibit the proliferation and invasion of NSCLC cells by suppressing the Wnt/beta-catenin signaling pathway.
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The expression level of PFTK1 was correlated with tumor grade, FIGO stage, lymph node metastasis of EOC patients as well as poor prognosis.
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Knockdown of PFTK1 inhibited the proliferation and invasion of pancreatic cancer cells as well as the EMT progress by suppressing the PI3K/Akt signaling pathway.
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PFTK1 overexpression promoted proliferation, migration and invasion of gastric cancer cells, while PFTK1 knockdown led to the opposite results.
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Knockdown of PFTK1 increases E-cadherin expression, decreases vimentin expression and inhibits migration of glioma cells.
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Up-regulated PFTK1 might promote breast cancer progression.
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Cigarette smoke down regulates CDK14 levels and impairs Wnt signaling.
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findings indicate that brain PP-1I associates with and is regulated by the associated protein kinases C-TAK1 and PFTK1
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binding of CCNY to 14-3-3 significantly enhanced the association between CCNY and CDK14
