Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C1522282 (EMT)
 2,868 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intestinal stem cells are monoclonal, multipotent cells residing in the niches of intestinal cripts where they regulate colonic epithelial turnover. It has been recently demonstrated that alterations in signalling transduction of the intestinal stem cells is implicated in the onset of colorectal cancer. Chronic inflammation may be one of the mechanisms involved in cancerogenesis because failure of resident stem cells in repairing the epithelial damage for the chronic insult, recruits bone marrow stem cells, which can develop genetic mutations due to the inflamed environment, leading to cancer. The main mutations associated with colorectal cancer affect the most important cellular signalling pathway, the Wnt. Mutations of adenomatous polyposis coli (APC) tumor suppressor gene and b catenin oncogene are the most common and severe alterations of this pathway. Tissue invasion and metastatization require a two-side transition of cancer stem cells, from epithelial phenotypes to mesenchimal one (epithelial transition tumor, EMT) and from the mesenchimal phenotype to the epithelial one (mesenchymal transition tumor, MET) under the regulatory effects of the environment, the intracellular b catenin distribution and P16 cell cycle inhibitor. Stem cells provide normal intestinal epithelial turnover, but may also promote intestinal cancerogenesis, and, since the cancer stem cells during the mesenchimal status are resistant to the chemotherapy (which is active only on proliferating cells), they represent the true target of future therapeutic approaches in oncology.
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PMID:[Stem cells and colorectal cancerogenesis: new insight]. 2054 78

Small nucleolar RNA host gene 7 (SNHG7) is a newly recognized oncogenic Long non-coding RNA (lncRNA) in most human cancers. In gastric cancer, SNHG7 has been suggested to enhance cell proliferation and suppressed apoptosis through down-regulating P15 and P16 expression, but the effect of SNHG7 on gastric cancer cell migration and invasion was still unknown. In our study, we aimed to estimate the relationship between SNHG7 expression and clinical and pathological characteristics, and explore the effect of SNHG7 on gastric cancer cell migration and invasion. In our study, the levels of SNHG7 expression in gastric cancer tissues and cell lines were severally higher than in normal adjacent tissues and gastric mucosal epithelial cells. Moreover, high SNHG7 expression was positively correlated with TNM stage, depth of invasion, lymph-node metastasis and distant metastasis in gastric cancer patients. Furthermore, the multivariate Cox proportional hazard analysis further showed high SNHG7 expression was an independent poor prognostic factor for overall survival in gastric cancer patients. The studies in vitro revealed that SNHG7 directly binds to miR-34a and negatively regulates miR-34a expression, and SNHG7 enhances gastric cancer cell migration and invasion through suppressing miR-34a-Snail-EMT axis. In conclusion, SNHG7 functions as oncogenic lncRNA in gastric cancer and may be a potential therapeutic target for gastric cancer patients.Abbreviations: lncRNA: Long non-coding RNA; SNHG7: Small nucleolar RNA host gene 7; EMT: Epithelial mesenchymal transition; TNM: Tumor-Lymph Node-Metastasis.
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PMID:SNHG7 accelerates cell migration and invasion through regulating miR-34a-Snail-EMT axis in gastric cancer. 3181 18