Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mitogen-activated protein kinase kinase kinase 3 (MAP3K3) is ubiquitously expressed in numerous tissues and is activated by various extracellular stimuli to regulate processes, such as cell proliferation and differentiation. Recent studies have identified potentially pathologic conditions of MAP3K3 as an oncogene that promotes tumor progression and metastasis in a number of malignancies. However, the clinical significance of MAP3K3 expression in ovarian carcinoma (OC) remains unclear. In this study, the correlation between MAP3K3 expression and OC prognosis was assessed by immunohistochemistry. MAP3K3 overexpression was observed in 59.1% (55/93) of OCs and was significantly associated with histological type and grade, chemotherapy response, and challenge model (P < .05, respectively). MAP3K3 overexpression was also used as an independent prognostic marker for decreased disease-free survival and overall survival. In OC cell lines, MAP3K3 expression was evaluated by Western blot analysis, quantitative real-time polymerase chain reaction, and immunofluorescence. High MAP3K3 expression is significantly detected in SKOV3, C13*, and A2780 cells. All these findings suggested that MAP3K3 overexpression is an independent poor prognostic indicator of OC and can be a clinically effective biomarker of OC.
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PMID:MAP3K3 overexpression is associated with poor survival in ovarian carcinoma. 2699 51

Despite the recent development of treatment strategies for nasopharyngeal carcinoma, the effective management of this disease remains a challenging clinical problem. A better understanding of the regulatory roles of miR-194 and mitogen-activated protein kinase kinase kinase 3 (MAP3K3) in the nasopharyngeal-carcinoma-related gene network is required to address this issue. Here, we measured relative expression of miR-194 in human nasopharyngeal carcinoma tissues and normal epithelial tissues by quantitative real time PCR. We transfected cultured CNE-1 and C666-1 cells with miR-194 mimics, and then examined the effects on cell proliferation, cell migration and invasion. Luciferase reporter assay was used to validate the putative binding between miR-194 and MAP3K3. We then examined the effect of knockdown and overexpression of MAP3K3 on cell tumorigenesis. Expression of miR-194 is significantly down-regulated in nasopharyngeal carcinoma specimens and tumor cell lines when compared with normal controls. In addition, miR-194 suppressed tumor cell proliferation and viability, as well as migration and invasion of carcinoma cells. We found that miR-194 binds the 3' untranslated region of MAP3K3, and knockdown of miR-194 inhibited nasopharyngeal carcinoma cell proliferation, migration and invasion. In accordance, overexpression of MAP3K3 reversed the inhibitory effects of miR-194 in carcinoma cells. This study suggests that expression of miR-194 is down-regulated in nasopharyngeal carcinoma, and that miR-194 can directly target MAP3K3 to regulate tumor progression. Given the pivotal involvement of MAP3K3 in nasopharyngeal carcinoma development, targeting miR-194 may be a novel strategy for the treatment of nasopharyngeal carcinoma.
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PMID:MiR-194 regulates nasopharyngeal carcinoma progression by modulating MAP3K3 expression. 3065 73