Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.22 (cdc2)
 8,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aim: We aimed to study the role of CKAP4 in clear cell renal cell carcinoma (ccRCC), which is not reported previously. Method: In silico exploration and validation using immunohistochemistry in ccRCC samples were used to identify the impact of CKAP4 expression on clinicopathological parameters. In vitro and in vivo studies were carried out to recapitulate the role of CKAP4 in ccRCC cell lines and animal models. Results: Overexpression of CKAP4 occurred in 5% of ccRCC patients, who had significantly worsened prognosis. Increased CKAP4 expression was significantly associated with TNM staging and Fuhrman grade. Pathway analysis for genes coexpressed with CKAP4 in ccRCC unanimously revealed significant cell cycle progression at G2/M phase. Expressions of CCNB1 and CCNB2 were correlated with CKAP4 expression. Genetic upregulation of CKAP4 significantly increased proliferation, cell invasion and migration in ccRCC cell lines, and vice versa for CKAP4 silencing. CKAP4 silencing also significantly increased cell population at G2/M phase, while not influencing cell apoptosis. Silencing or upregulation of CKAP4 resulted in decreased or increased CCNB1/2 expressions, respectively. CCNB1/CDK1 inhibitor significantly inhibited colony formation ability and in vivo tumor growth of RCC cells with CKAP4 overexpression. Conclusion: Upregulation of CKAP4 was associated with worsened characteristics of ccRCC. CKAP4 was related with CCNB signaling in ccRCC, which supported a role for CCNB/CDK inhibitor for ccRCC with such genotype.
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PMID:Overexpression of CKAP4 is Associated with Poor Prognosis in Clear Cell Renal Cell Carcinoma and Functions via Cyclin B Signaling. 2918 77

In this study, we planned to investigate the function and potential mechanisms of Alpha-1,3-mannosyltransferase (ALG3) in oral squamous cell carcinoma (OSCC). Data from TCGA were used to analyze ALG3 expression and its effect on the prognosis of patients with OSCC. KEGG enrichment analysis was applied to explore the pathways related to ALG3. ALG3 expression was measured by qPCR and Western blot. Cell counting kit-8, colony formation, and transwell assays were implemented to detect the effects of ALG3 on malignant biological properties of OSCC cells. The expression of key proteins related to CDK-Cyclin pathway was detected by Western blot. The expression of ALG3 in OSCC samples was higher than that of the control samples, and the increase of ALG3 expression was related to unfavorable prognosis of OSCC patients. Additionally, the elevated expression of ALG3 was associated with pathological stage, lymph node metastasis, and primary lesion in OSCC patients. ALG3 depletion blocked the growth and movement of OSCC cells, while over-expression ALG3 reversed these phenomena. Moreover, exhaustion of ALG3 resulted in decreased expression of MCM7/CCNB2/CDK1/PCNA, while these phenomena were inversed after ALG3 up-regulation. The enhancement of ALG3 expression promoted the aggressive biological behaviors of OSCC cells probably by promoting CDK-Cyclin pathway.
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PMID:ALG3 contributes to the malignant properties of OSCC cells by regulating CDK-Cyclin pathway. 3308 11