Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.22.62 (caspase-9)
 7,507 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study aimed to analyze the expression, clinical significance of epithelial membrane protein-1 (EMP1) in nasopharyngeal carcinoma, and the biological effect in its cell line by EMP1 overexpression. Immunohistochemistry and Western blot were used to analyze the EMP1 protein expression in 75 cases of nasopharyngeal cancer and 31 cases of normal tissues to study the relationship between EMP1 expression and clinical factors. Recombinant lentiviral vector was constructed to overexpress EMP1 and then infect nasopharyngeal cancer CNE2 cell line. Quantitative real-time RT-PCR and Western blot were used to detect the mRNA level and protein of EMP1. MTT assay, cell apoptosis, migration, and invasion assays were also conducted to determine the influence of the upregulated expression of EMP1 that might be found on CNE2 cells' biological effect. Immunohistochemistry and Western blot: The level of EMP1 protein expression was found to be significantly lower in nasopharyngeal cancer tissue than in the normal tissues (P < 0.05). Decreased expression of EMP1 was significantly correlated with T stages, lymph node metastasis, clinic stage, and histological grade of patients with nasopharyngeal cancer (P < 0.05). Meanwhile, the loss of EMP1 expression correlated significantly with poor overall survival time by Kaplan-Meier analysis (P < 0.05). The result of biological function has shown that CNE2 cell-transfected EMP1 had a lower survival fraction, higher cell apoptosis, significant decrease in migration and invasion, higher caspase-9, and lower vascular endothelial growth factor C protein expression compared with CNE2 cell-untransfected EMP1 (P < 0.05). EMP1 expression decreased in nasopharyngeal cancer and correlated significantly T stages, lymph node metastasis, clinic stage, histological grade, and poor overall survival, suggesting that EMP1 may play important roles as a negative regulator to nasopharyngeal cancer cell.
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PMID:EMP1 inhibits nasopharyngeal cancer cell growth and metastasis through induction apoptosis and angiogenesis. 2429 52

This study aimed to analyze the expression, clinical significance of f epithelial membrane protejn-1 (EMP-1) in prostate carcinoma, and the biological effect in its cell line by EMP1 overexpression. Immunohistochemistry and Western blot were used to analyze EMP1 protein expression in 76 cases of prostate cancer and 34 cases of normal tissues to study the relationship between EMP1 expression and clinical factors. EMP1 lentiviral vector and empty vector were respectively transfected into prostate cancer PC-3 cell line. Quantitative real-time reverse transcription polymerase chain reaction and Western blot were used to detect the mRNA level and protein of EMP1. 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay, migration, and invasion assays were also conducted as to the influence of the upregulated expression of EMP1 that might be found on PC-3 cell biological effect. Immunohistochemistry: The level of EMP1 protein expression was found to be significantly lower in prostate cancer tissue than normal tissues (P < 0.05). Western blot: The relative amount of EMP1 protein in prostate cancer tissue was found to be significantly lower than in normal tissues (P < 0.05). The level of EMP1 protein expression was not correlated with age and prostate-specific antigen (PSA) concentration (P > 0.05), but it was correlated with T stages, lymph node metastasis, clinic stage, and Gleason score (P < 0.05). The result of biological function shown that PC-3 cell transfected EMP1 had a lower survival fraction, higher cell apoptosis, significant decrease in migration and invasion, higher caspase-9, and lower VEGFC protein expression compared with PC-3 cell untransfected EMP1 (P < 0.05). EMP1 expression decreased in prostate cancer and correlated significantly T stages, lymph node metastasis, clinic stage, and Gleason score, suggesting that EMP1 may play important roles as a negative regulator to prostate cancer PC-3 cell by regulating the expression of regulation of caspase-9 and VEGFC protein.
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PMID:EMP1 regulates caspase-9 and VEGFC expression and suppresses prostate cancer cell proliferation and invasion. 2433 11

This study aimed to analyze the expression, clinical significance of epithelial membrane protein 1 (EMP1) in breast carcinoma and the biological effect in its cell line by EMP1 overexpression. Immunohistochemistry and western blot were used to analyze EMP1 protein expression in 67 cases of breast cancer and 35 cases of normal tissues to study the relationship between EMP1 expression and clinical factors. Quantitative real-time RT-PCR and western blot were used to detect the mRNA level and protein of EMP1. MTT assay, migration and invasion assays were also conducted as to the influence of the upregulated expression of EMP1 that might be found on MCF-7 cell biological effect. The relative amount of EMP1 protein in breast cancer tissue was found to be significantly lower than in normal tissues (P < 0.05). The level of EMP1 protein expression was correlated with T stages, lymph node metastasis, clinic stage, and histological grade (P < 0.05). Meanwhile, loss of EMP1 expression correlated significantly with poor overall survival time by Kaplan-Meier analysis (P < 0.05). The result shown that MCF-7 cell transfected EMP1 had a lower survival fraction, higher cell apoptosis, significant decrease in migration and invasion, higher caspase-9, and lower VEGFC protein expression compared with MCF-7 cell untransfected EMP1 (P < 0.05). EMP1 expression decreased in breast cancer and correlated significantly with lymph node metastasis, clinic stage, histological grade, and poor overall survival, T stages, suggesting that EMP1 may play important roles as a negative regulator to breast cancer MCF-7 cell by regulating the expression of caspase 9 and VEGFC protein.
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PMID:EMP1, a member of a new family of antiproliferative genes in breast carcinoma. 2440 72