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Epithelial Mesenchymal Transition as Targets for Cancer Therapy

Author

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  • Krishnaveni M

    (Department of Biochemistry, Periyar University, India)

Abstract

Most of the primary epithelial cancers are developed by increased epithelial cell proliferation and angiogenesis. When these cancer cells broke, they shed their contents in to the blood stream as well as in to the lymphatic vessels and stay at sites called as secondary site via metastasis mediated by epithelial mesenchymal transition giving cell a mesenchymal nature that are more prevalent in cancers of various types. Irreversible mutation and reversible epigenetic changes like methylation in DNA, histone modifications, altered miRNA also cause cancer as they are prone to deletion, amplification, recombination. Epithelial mesenchymal transition develops resistance to treatment drugs. Hence, using EMT as targets for cancer will be of much useful and in the present review few targets that could alter EMT is discussed. So, any natural compound that could act on the process of EMT i.e able to inhibit the transition in to mesenchymal cell in order to maintain architecture and adhesive property of cell.

Suggested Citation

  • Krishnaveni M, 2017. "Epithelial Mesenchymal Transition as Targets for Cancer Therapy," Novel Approaches in Drug Designing & Development, Juniper Publishers Inc., vol. 3(1), pages 14-18, November.
    • Handle: RePEc:adp:jnapdd:v:3:y:2017:i:1:p:14-18
    DOI: 10.19080/NAPDD.2017.03.555604
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    References listed on IDEAS

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    1. Derek C. Radisky & Dinah D. Levy & Laurie E. Littlepage & Hong Liu & Celeste M. Nelson & Jimmie E. Fata & Devin Leake & Elizabeth L. Godden & Donna G. Albertson & M. Angela Nieto & Zena Werb & Mina J., 2005. "Rac1b and reactive oxygen species mediate MMP-3-induced EMT and genomic instability," Nature, Nature, vol. 436(7047), pages 123-127, July.
    2. Li Ma & Julie Teruya-Feldstein & Robert A. Weinberg, 2007. "Tumour invasion and metastasis initiated by microRNA-10b in breast cancer," Nature, Nature, vol. 449(7163), pages 682-688, October.
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