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)

Recent studies have shown that many molecular mechanisms, such as the EGFR, AKT, STAT3, and beta-catenin pathways, are involved in glioma. However, the prognosis of the disease remains poor. Explorations of the underlying mechanisms of glioma and identification of effective markers for early diagnosis and accurate prognostication remain important today. In this study, we employed survival analysis to determine that TPM3 overexpression was significantly associated with high-grade gliomas and higher mortality. Using microarray combined with Pearson correlation analysis, we found that TPM3 was positively correlated with the expression of MMP family members and EMT-like activators. Reduction of TPM3 (via TPM3-siRNA) inhibited cellular invasion and migration and decreased MMP-9 and SNAI1 levels in glioma cells. To the best of our knowledge, our work is the first to show that TPM3 plays a critical role in the progression of gliomas and provides novel insights into the key roles of MMP family members and EMT-like activators that mediate TPM3 functional signaling for glioma regulation.
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PMID:TPM3, a strong prognosis predictor, is involved in malignant progression through MMP family members and EMT-like activators in gliomas. 2491 5

Background: Pancreatic cancer is one of the most aggressive human malignancies that is associated with early metastasis and chemoresistance. Tropomyosin (TPM) is an indispensable regulatory protein for muscle contraction, Abnormal expressions of TPM gene are closely related to the carcinogenesis and metastasis of malignant tumors. Purpose: In this experiment, a monoclonal stable transfected cell line was established by the knock-down of TMP3 expression in PANC-1 cells with the lentivirus method, and the impacts of the downregulated TPM3 gene expression on the EMT-related molecules and biological behaviors of PANC-1 cells were explored. Methods: Based on the TPM3 gene sequence, we designed the RNA interference sequence, constructed and screened out the recombinant plasmid segment TPM3-shRNA with the optimal silencing effect, and carried out lentivirus titer determination and packaging. The recombinant lentiviral interference vector LV-TPM3-shRNA was transfected into PANC-1 cells; the transfection efficiency was then evaluated to screen out the monoclonal stable transfected PANC-1 cell line with downregulated TPM3 expression. The qRT-PCR and Western blot were used to detect the changes in the gene- and protein-levels expressions of EMT-related transcription factors in the target cell line and to respectively test the variations of the invasion and proliferation capacities. Results: It is shown that the monoclonal stable transfected PANC-1 cell line with downregulated TPM3 expression was successfully established with the recombinant lentiviral vector. After knocking down the expression of TPM3 gene in PANC-1 cells, EMT occurred in the cells; the cell phenotype showed malignant transformation, and the in vitro biological behaviors of the cells (such as proliferation and invasion) were enhanced to different degrees. Conclusion: It is indicated that the TPM3 gene can be a potential target spot for the treatment of pancreatic cancer.
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PMID:Research on the establishment of a TPM3 monoclonal stable transfected PANC-1 cell line and the experiment of the EMT occurrence in human pancreatic cancer. 3137 95