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Awakening the sleeping/cancer-protecting angels in mutant p53-expressing human tumors: Emodin, isolated from Rhubarb and others,  increases the expression of tumor suppressors genes, such as PTEN, PDCD4, TA-p73, TAp63, p53, and others, induces regression of p53-mutated human tumors, via down regulation of its target gene, 6/July/2018, 10.45 am

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From Significance of the study to Public health relevance

Given that: (1) cancer suppressor p53 is mutated in more than 50% of human cancers of different tissue origin; (2) p53 pathway is altered in about 80% of tumors.; (3) our understanding is incomplete in terms of molecular targets and the oncogenic/malignant pathways involved in mutant p53-overexpressing tumors; (4) cancer causes the highest economic loss compared to all the known causes of death worldwide; and (5) cancer causes the considerable economic loss worldwide, there is an urgent need to find: (i) a cheaper alternative to the existing expensive drugs; (ii) a side-effect-free natural product-based drug; and (iii) a way to effectively treat and stall metastatic progression and relapse of mutant p53-overexpressing human cancers.


From therapeutic strategy to Research Findings:

(i) Therapeutic strategy: 

This study suggests a therapeutic strategy for stalling the progression of p53-deficient/deleted or mutant-p53 expressing metastatic cancers. By activating tumor suppressor p53’s unmutated “homologous protein such as TAp73/p63” in p53-deficient or mutant-p53 expressing metastatic cancer cells, one can stall their progression.

(ii) Research findings:  

Emodin has been shown to function as an anticancer agent in a number of cancers. However, the mechanism of action remains largely unknown.

Figure 1. Mechanistic insight into how  Emodin functions as an anticancer/antimetastatic agent in mutant p53-expressing tumors.  Emodin,  by activating tumor/metastasis suppressor genes, such as PTEN, PDCD4, TA-p73, TAp63, p53 and others, in  metastatic tumors, it may inhibit the progression of mutant-p53 expressing human cancers

Figure 2. Emodin functions as an anti-tumor/metastatic agent through induction of tumor/metastatic suppressor genes, such as PTEN, PDCD4, p53, TAp63, TAp63

This study suggests that Emodin may function as an anti-cancer/metastasis agent by increasing the expression a number of tumor/metastasis suppressor genes

Emodin, by increasing the expression of its target gene, it may increase the expression of tumor/metastasis suppressors genes, such as INK4a, BTG2, TA-p73, TAp63, p53, and others. Thereby, it may inhibit the migration and invasion of metastatic cancer cells expressing mutant-p53 (figure1).

 


Therapeutic opportunity:

Given the ability of Emodin to induce the expression of a number of tumor/metastasis suppressor genes, it may be used, either alone or in combination with other anticancer drugs, to inhibit the progression of p53-mutated invasive metastatic tumors. Taken together, this study suggests, for the first time, that oncologists may consider treating terminally ill metastatic cancer patients with Emodin, as it may stall the progression of advanced metastatic cancers. Given its low cost compared to other anti-cancer/metastatic agents, it may be a prefered anti-cancer/metastatic agent (figure 2).


Details of the research findings

Idea Proposed/Formulated by: Dr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

Amount: $300#

Undisclosed mechanistic information: How Emodin increases the expression of tumor suppressor genes, such as PTEN, PDCD4, TAp63, p53, and others,  in mutant p53 expressing cancer cells?

For purchase and payment details, you may reach us at admin@genomediscovery.org

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References:

Web: http://genomediscovery.org or http://newbioideas.com

Citation: Boominathan, L., Awakening the sleeping/cancer-protecting angels in mutant p53-expressing human tumors: Emodin, isolated from Rhubarb and others,  increases the expression of tumor suppressors genes, such as PTEN, PDCD4, TA-p73, TAp63, p53, and others, induces regression of p53-mutated human tumors, via down regulation of its target gene, 6/July/2018, 10.45 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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