Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our previous study has suggested an oncogenic role of eIF-5A2 in ovarian tumorigenesis. Abnormalities of eIF-5A2, however, in colorectal carcinoma are unclear. In this study, amplification and overexpression of eIF-5A2 in colorectal carcinoma were studied by fluorescence in situ hybridization and immunohistochemistry using colorectal carcinoma tissue microarrays, including 139 primary colorectal carcinomas and their adjacent normal mucosa, 22 paired premalignant adenomas, and 42 metastatic tumors. The immunohistochemistry results showed that overexpression of EIF-5A2 was detected in none of normal epithelial mucosa, 35.3% of colorectal adenomas, 53.2% of primary colorectal carcinomas, and 67.6% of metastases. Amplification of eIF-5A2 was detected in 15.8% (16/101) of informative colorectal carcinomas, and most of them showed overexpression of EIF-5A2. In primary colorectal carcinomas, the frequency of EIF-5A2 overexpression was significantly higher in colorectal carcinomas with lymphovascular invasion (61.2%) than that in colorectal carcinomas without lymphovascular invasion (36.6%, P < .05). In addition, significant positive associations were found between EIF-5A2 overexpression and the tumors' later pN and pM stages, as well as increased tumor cell proliferation (P < .05). These findings suggest that overexpression of EIF-5A2 in colorectal carcinomas may be important in the acquisition of a metastatic phenotype and plays an important role in colorectal carcinoma development and progression.
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PMID:Overexpression of EIF-5A2 is associated with metastasis of human colorectal carcinoma. 1794 76

Metastasis is the primary cause of prostate cancer (CaP)-related death. We investigate the molecular, pathologic and clinical outcome associations of EphA6 expression and CaP metastasis. The expression profiling of Eph receptors (Ephs) and their ephrin ligands was performed in parental and metastatic CaP cell lines. Among Ephs and ephrins, only EphA6 is consistently overexpressed in metastatic CaP cells. Metastatic potential of EphA6 is assessed by RNAi in a CaP spontaneous metastasis mouse model. EphA6 knock-down in human PC-3M cells causes decreased invasion in vitro and reduced lung and lymph node metastasis in vivo. In addition, knock-down of EphA6 decreases tube formation in vitro and angiogenesis in vivo. EphA6 mRNA expression is higher in 112 CaP tumor samples compared with benign tissues from 58 benign prostate hyperplasia patients. Positive correlation was identified between EphA6 expression and vascular invasion, neural invasion, PSA level, and TNM staging in CaP cases. Further, genome-wide gene expression analysis in EphA6 knock-down cells identified a panel of differentially regulated genes including PIK3IPA, AKT1, and EIF5A2, which could contribute to EphA6-regulated cancer progression. These findings identify EphA6 as a potentially novel metastasis gene which positively correlates with CaP progression. EphA6 may be a therapeutic target in metastatic CaP.
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PMID:EphA6 promotes angiogenesis and prostate cancer metastasis and is associated with human prostate cancer progression. 2604 87

Long non-coding RNA termed GAS6 antisense RNA 1 (GAS6-AS1) plays an essential role in gastric and non-small cell lung cancers. Nonetheless, the function of GAS6-AS1 in hepatocellular carcinoma (HCC) has not been so far studied in detail. In this study, reverse-transcription quantitative PCR was performed to measure GAS6-AS1 expression in HCC samples. A series of functional experiments, including MTT assay, colony formation assay, flow-cytometric analysis, and transwell migration and invasion assays, was performed to determine the influence of GAS6-AS1 knockdown on the malignant phenotype of HCC. The results showed that GAS6-AS1 was significantly upregulated in HCC tissue samples and cell lines. Increased GAS6-AS1 expression was associated with tumor size, Edmondson grade, and Tumor-Node-Metastasis (TNM) stage among patients with HCC. The overall survival of patients with HCC characterized with high expression of GAS6-AS1 was significantly shorter in comparison to that of patients with low level of GAS6-AS1. Functional experiments indicated that knockdown of GAS6-AS1 suppressed HCC cell proliferation, colony formation, migration, and invasion in vitro; promoted apoptosis in vitro; and decreased tumor growth in vivo. Of note, GAS6-AS1 was validated as a competing endogenous RNA (ceRNA) for microRNA-585 (miR-585) and consequently increased the expression of eukaryotic translation initiation factor 5A2 (EIF5A2). Finally, rescue experiments confirmed the association among GAS6-AS1, miR-585, and EIF5A2 in HCC cells. Our study provides substantial evidence that the GAS6-AS1/miR-585/EIF5A2 pathway plays an important role in HCC progression and that might be considered as a potential target for therapeutic approaches in HCC.
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PMID:Long non-coding RNA GAS6-AS1 acts as a ceRNA for microRNA-585, thereby increasing EIF5A2 expression and facilitating hepatocellular carcinoma oncogenicity. 3208 66