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- W4387573703 abstract "Epithelial-mesenchymal transition (EMT) induces dynamic changes in the cellular organization leading to functional changes in cell migration, invasion, and metastasis. Neoplastic cells with specific genetic and epigenetic alterations undergo EMT. While the epithelial cell comprises various classes of cell junctions, including desmosomes, adherens junctions (AJ), tight junctions (TJ), and gap junctions (GJ), TJs are considered central players in regulating epithelial cell function. The TJ proteins include junctional adhesion molecules (JAM), Pals1 (Proteins Associated with Lin Seven 1), cingulin, MUPP1 (multi-PDZ domain protein 1), tricellulin, and ZO1, ZO-2, ZO-3 (Zona occludens). Claudins have been found to have abnormal expressions in a variety of malignancies. Differential expression of TJ proteins has been observed in various malignancies, including prostate, lung, breast, ovarian, esophageal, colorectal, and gastric cancers. Disruption in the expression of TJ proteins results in the EMT phenotype associated with loss of cell-cell adhesion and dissociation of cells from primary tumor followed by invasion and metastasis to distant organs. In addition, claudins and occludins, the essential TJ proteins, also mediate various crucial functions in the cell. TJ proteins are also hepatocyte entry factors for the hepatitis-C virus (HCV), a leading cause of liver disease and cancer worldwide. This chapter comprehensively discusses the current knowledge on the involvement of TJ proteins in the EMT and metastasis of various cancers." @default.
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- W4387573703 date "2023-01-01" @default.
- W4387573703 modified "2023-10-13" @default.
- W4387573703 title "Tight Junctions, Epithelial-Mesenchymal Transition, and Cancer Metastasis" @default.
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- W4387573703 doi "https://doi.org/10.1007/978-981-99-2415-8_3" @default.
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