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Molecular therapy for Metastatic cancers: Metformin, an anti-hyperglycemic drug, increases the expression of tumor/metastatic suppressors BTG2 and INK4a , inhibits cell cycle progression, and suppresses migration, invasion and metastasis of cancer cells via up regulation of its target gene, 23/January/2018, 5.16 am

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From significance of the study to Public health relevance: 

Given that: (i) each year nearly 14 million people are diagnosed with cancer globally, and little more than half of them will die; (ii) cancer deaths globally are expected to be doubled by 2030; (iii) most of the cancer patients die due to metastasis; (iv) cancer treatment causes the highest economic loss compared to all the known causes of death worldwide, there is an urgent need to find: (i) bio-molecules that drive metastatic process; and the the way to prevent their expression; (ii) a way to activate immune system to combat cancer (Cancer immunotherapy); (ii) a cheaper alternative to the existing expensive anticancer drugs; (ii) a side-effect-free natural product-based drug; (iii) increase the therapeutic index of anticancer drugs; and (iv) a way to effectively treat and prevent metastatic progression and relapse of advanced/drug-resistant cancers.


Research findings to Therapeutic opportunity: 

This study suggests, for the first time, that  the anti-diabetic medication Metformin, by regulating the expression of its target genes, it may increase the expression of tumor/metastatic suppressors BTG2 and INK4a  (fig. 1).

 

Thereby, it may: (a) inhibit cell cycle progression; and (b) suppress migration, invasion and metastasis of cancer cells.   [easy_payment currency=”USD”]

Given the mechanism of action of Metformin, it may be an ideal anti-metastatic agent to  (i) increase the expression of metastasis suppressor genes in tumors; (ii) inhibit the progression of metastatic tumors; and (ii) enhance the efficacy of Cancer therapy.

Taken together, this study suggests that oncologists may consider treating terminally ill metastatic cancer patients with Metformin, to stall the progression of advanced metastatic cancers.


Details of the research findings: 

Idea Proposed/Formulated (with experimental evidence) by:

Dr L Boominathan Ph.D

Amount: $5#

Undisclosed mechanistic information: How Torasemide increases the expression of  tumor/metastatic suppressors BTG2 and INK4a 

Fig1. Mechanistic insights into how the anti-hyperglycemic medication Metformin functions as an anti-metastasis agent. Metformin increases the expression of tumor/metastatic suppressors BTG2 and INK4a via up regulation of its target genes

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References: 

CitationBoominathan, L., Molecular therapy for Metastatic cancers: Metformin, an anti-hyperglycemic drug, increases the expression of tumor/metastatic suppressors BTG2 and INK4a , inhibits cell cycle progression, and suppresses migration, invasion and metastasis of cancer cells via up regulation of its target gene, 23/January/2018, 5.16 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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