Molecular therapy for Metastatic human tumors: Ndfip1 inhibits cellular proliferation, invasion and metastasis by increasing the expression of tumor suppressor TAp63 via down regulation of its target gene, 5/May/2015, 17.26

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A study from the Cell Pathology Division, The Children’s Hospital of Philadelphia, Philadelphia, USA shows that “TGF-β induces the expression of the adaptor Ndfip1 to silence IL-4 production during iTreg cell differentiation.” This study was published in the 15 November  2009 issue of the journal “Nature Immunology” [the number 1 journal in Immunology with an I.F of 24.973] by Prof. Oliver PM, Beal and others.

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Molecular therapy for Metastatic human tumors: Ndfip1 inhibits cellular proliferation, invasion and metastasis by increasing the expression of tumor suppressor p53 homogue TAp63 via down regulation of its target gene. 

Significance:

Cancer suppressor p53 is mutated in more than 50% of tumors of different origin, while its pathway is altered in about 80% of human tumors. This study suggests a therapeutic strategy as to how p53-deficient or mutant p53 expressing human cancers can be cured by increasing the expression of its homologous protein such as TAp63α. Adoptor protein Ndfip1, by decreasing the expression of its target gene, it may increase the expression of TAp63. Thus, pharmacological formulations encompassing “Ndfip1 activators” may be used to stall metastatic progression of p53-deficient or mutant p53 expressing human tumors. 

Undisclosed information: How Ndfip1 increases the expression of TAp63

Idea Proposed/Formulated byDr L Boominathan Ph.D.

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To citeBoominathan, Molecular therapy for Metastatic human tumors: Ndfip1 inhibits cellular proliferation, invasion and metastasis by increasing the expression of tumor suppressor TAp63 via down regulation of its target gene, 5/May/2015, 17.26,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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