Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to investigate whether indomethacin and NGX6 synergistically inhibit the growth and invasiveness of human colon cancer cells (HT-29 and SW620) and to elucidate the molecular mechanism of their action. Cell proliferation was assessed by MTT assay. Cell apoptosis was assessed by acridine orange/ethidium bromide staining (AO-EB) and annexin-V-FITC/PI assay. Invasive behaviors of colorectal cancer cells were examined by cell adhesion, migration, and invasion assays. Gap junctional intercellular communication (GJIC) was assessed by the scrape-loading/dye transfer technique. The subcellular localization and expression of beta-catenin protein was examined by immunofluorescence staining and western blot analysis, respectively. Indomethacin and NGX6 had a synergistic effect on inhibiting proliferation and invasiveness of colon cancer HT-29 and SW620 cells, restoring GJIC of HT-29 and SW620, and suppressing translocation of beta-catenin from the nucleus and cytoplasm to the plasma membrane. However, they did not have synergistic effects on enhancing apoptosis and suppressing extracellular matrix adhesion of HT-29 and SW620 cells. Indomethacin and NGX6 inhibit the proliferation and invasiveness of HT-29 and SW620 colon cancer cells by attenuating the WNT/ss-catenin signaling pathway.
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PMID:Synergistic effect of indomethacin and NGX6 on proliferation and invasion by human colorectal cancer cells through modulation of the Wnt/beta-catenin signaling pathway. 1935 43

Colon cancer is a common malignant tumor that is associated with increased morbidity and mortality. Nasopharyngeal carcinoma-associated gene 6 (NGX6) is a novel candidate suppressor gene of tumor metastasis, which is down-regulated in colon cancer. This study was designed to investigate the roles of NGX6 on the growth and invasiveness of human colon cancer cell line, HT-29, and to elucidate the molecular mechanism of their action. Results showed that NGX6 could inhibit the invasiveness and extracellular matrix adhesion of HT-29 cells and restore the gap junctional intercellular communication of cells. Moreover, NGX6 could suppress the translocation of beta-catenin from nucleus and cytoplasm to plasma membrane, inhibit the activity of TCF4 transcript factor, and down-regulate the expression of Wnt-direct-targeted genes c-myc, cyclin D1 and COX-2. We suggested that NGX6 inhibits cell invasion and adhesion through the suppression of Wnt signal pathway in colon cancer.
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PMID:NGX6 inhibits cell invasion and adhesion through suppression of Wnt/beta-catenin signal pathway in colon cancer. 2070 83

Nasopharyngeal carcinoma-associated gene 6 (NGX6) was shown to be a novel putative tumor suppressor gene in colon cancer. The purpose of this study is to investigate its role in regulation of miRNA expression for in the hopes of translating this data into a novel strategy in control of colon cancer. In this study colon cancer HT-29 cells were stably transfected with NGX6 or vector-only plasmid and then subjected to miRNA array analysis, and Q-RT-PCR was then used to verify miRNA array data. Then bioinformatic analyses using Sanger, Target Scan, and MicroRNA software were performed to obtain data on the target genes of each miRNA and define their function. Our results showed that 14 miRNAs were found to be differentially expressed in NGX6-transfected cells compared to the control cells. In particular, miR-126, miR-142-3p, miR-155, miR-552, and miR-630 were all upregulated, whereas miR-146a, miR-152, miR-205, miR-365, miR-449, miR-518c, miR-584, miR-615, and miR-622 were downregulated after NGX6 transfection. Q-RT-PCR confirmed all of these miRNAs, and invalidated miR-552 and miR-630. Furthermore, bioinformatic analyses of these 12 miRNAs, among these miRNAs, target genes of miR-615 are unclear, another 11 miRNAs produced a total of 254 potential target genes and further study showed that these genes together formed a regulatory network that contributes to apoptosis, mobility/migration, hydrolysis activity, and molecular signaling through targeting JNK and Notch pathways. Taken together, these results have suggested that NGX6 plays an important role in regulation of apoptosis, mobility/migration, and hydrolase as well as activity of JNK and Notch pathways through NGX6-mediated miRNA expression. Further investigation will reveal the function of these differentially expressed miRNAs and verify expression of the miRNA-targeted genes for development of novel strategies for better control of colon cancer.
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PMID:Differential miRNA expression and their target genes between NGX6-positive and negative colon cancer cells. 2085 56

Nasopharyngeal carcinoma-associated gene 6 (NGX6; syn. transmembrane protein 8B, TMEM8B) is a recently identified tumor suppressor gene. The underlying mechanisms by which the gene inhibits tumor development are not completely known. To further understand the function of the gene's protein product NGX6, in the present study, we employed two-dimensional difference gel electrophoresis to analyze the protein expression profiles of colon cancer HT-29 cells stably transfected with the gene NGX6. The differentially expressed proteins were selected and identified by matrix-assisted laser desorption/ionization coupled with time-of-flight tandem mass spectrometry. The results showed that 12 proteins were down-regulated and 4 were up-regulated in NGX6-transfected HT-29 cells, compared with vector-transfected HT-29 cells. The MS results were verified by western blot. Bioinformatic analysis showed that these proteins are involved in cell proliferation, metastasis, apoptosis, cytoskeletal structure, metabolism, and signal transduction, suggesting that NGX6 may inhibit colon cancer through the regulation of these biological processes.
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PMID:Tumor suppressor gene NGX6 induces changes in protein expression profiles in colon cancer HT-29 cells. 2264 48