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

Colorectal cancer (CRC) is the third form of cancer in both men and women. In Romania, the incidence of CRC in 2000 is 17.74 %ooo, in 2002 becoming the second cause of death. We reviewed a series of studies that are related to colon cancer and studied the epithelial-mesenchymal transition at the front of tumor invasion (EMT). Cellular phenotypic changes characteristic of EMT can be induced by the absence of transition cofactor (p300) involved in cellular regulation. Loss of syndecan-l marker is associated with local tumor stage and metastasis. Modulators of protein kinase resistance was associated with changes in genes involved in EMT (including vimentin hyperexpression) and genes involved in invasion (N-cadherin) with a decrease expression of genes involved in epithelial cell adhesion (E-cadherin). Progression in colon cancer is characterized by activating mutations in Ras genes and tumor growth factor action. Vimentin expression associated with EMT initiates molecular program. One of the characteristics of EMT is the loss of E-cadherin. TGF-p (transforming growth factor beta) induces epithelial-mesenchymal transition in colon cancer cell lines with the microsatellite stability, inducing cell invasion and migration. EMT is a critical early event involved in invasion and metastasis of colorectal cancer, characterized by the presence of markers specific to each phenotype, epithelial or mesenchymal. Multiple biomarkers involved in the induction of EMT may represent future therapeutic target in the treatment of colonic neoplasia.
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PMID:Colon cancer at the molecular level--usefulness of epithelial-mesenchymal transition analysis. 2370 Aug 97

ING5 belongs to the Inhibitor of Growth (ING) candidate tumor suppressor family. Previously, we have shown that ING5 inhibits invasiveness of lung cancer cells by downregulating EMT-inducing genes. However, the underlying mechanisms remain unclear. The aim of the study was to use integrated approach involving SILAC labeling and mass spectrometry-based quantitative proteomics to quantify dynamic changes of acetylation regulated by ING5 in lung cancer cells. Here, we have found that ING5 has a profound influence on protein lysine acetylation with 163 acetylation peptides on 122 proteins significantly upregulated and 100 acetylation peptides on 72 proteins downregulated by ING5 overexpression. Bioinfomatic analysis revealed that the acetylated proteins upregulated by ING5 located preferentially in nucleus to cytoplasm and were significantly enriched in transcription cofactor activity, chromatin binding and DNA binding functions; while those downregulated by ING5 located preferentially in cytoplasm rather than nucleus and were functionally enriched in metabolism, suggesting diverse functions of ING5 through differentially regulating protein acetylation. Interestingly, we found ING5 overexpression promotes p300 autoacetylation at K1555, K1558 and K1560 within p300 HAT domain, and two novel sites K1647 and K1794, leading to activation of p300 HAT activity, which was confirmed by accelerated acetylation of p300 target proteins, p53 at k382 and histone H3 at K18. A specific p300 HAT inhibitor C646 impaired ING5-increased acetylation of H3K18 and p53K382, and subsequent expression of p21 and Bax. In conclusion, our results reveal the lysine acetylome regulated by ING5 and provide new insights into mechanisms of ING5 in the regulation of gene expression, metabolism and other cellular functions.
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PMID:ING5 differentially regulates protein lysine acetylation and promotes p300 autoacetylation. 2941 18

Increasing evidence suggest that lncRNAs (long noncoding RNAs) play important roles in human cancer. Breast cancer is a heterogeneous disease and the potential involvement of lncRNAs in breast cancer remains unexplored. In this study, we characterized a novel lncRNA, RP1-5O6.5 (termed as RP1). We found that RP1 was highly expressed in breast cancer and predicted poor prognosis of breast cancer patients. Gain-of-function and loss-of-function assays showed that RP1 promoted the proliferation and metastasis of breast cancer cells in vitro and in vivo. Mechanistically, RP1 maintained the EMT and stemness states of breast cancer cells via repressing p27kip1 protein expression. RP1 combined with the complex p-4E-BP1/eIF4E to prevent eIF4E from interacting with eIF4G, therefore attenuating the translational efficiency of p27kip1 mRNA. Furthermore, we found that p27kip1 evidently downregulated Snail1 but not ZEB1 to inhibit invasion of breast cancer cells. Kruppel-like factor 5 (KLF5) was positively correlated with RP1 in breast cancer tissues. Moreover, we demonstrated that KLF5 recruited p300 to the RP1 promoter to enhance RP1 expression. Taken together, our findings demonstrated that KLF5-regulated RP1 plays an oncogenic role in breast cancer by suppressing p27kip1, providing support for the clinical investigation of therapeutic approaches focusing on RP1.
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PMID:KLF5 regulated lncRNA RP1 promotes the growth and metastasis of breast cancer via repressing p27kip1 translation. 3107 22