Awakening the sleeping/cancer-protecting angels in mutant p53-expressing human tumors: Act1 (Adaptor for IL-17 receptors) increases the expression of tumor suppressors genes, such as BTG2, TIMP3, p53, TAp63, TAp73, INK4a/ARF, and others, induces regression of p53-mutated human tumors, via down-regulation of its target gene, 5/October/2018, 11.28 pm

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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:  

This study suggests that Act1 (Adaptor for IL-17 receptors) may function as a tumor suppressor gene in mutant p53 expressing human cancers. 

Figure 1. Mechanistic insight into how  Act1 (Adaptor for IL-17 receptors) functions as an anticancer/antimetastatic agent in mutant p53-expressing tumors.  Act1 (Adaptor for IL-17 receptors),  by activating tumor/metastasis suppressor genes, such as BTG2, TIMP3, p53, TAp63, TAp73, INK4a/ARF and others, in metastatic tumors, it may inhibit the progression of mutant-p53 expressing human cancers

Figure 2.  Act1 (Adaptor for IL-17 receptors)  functions as an anti-tumor/metastatic agent through induction of tumor/metastatic suppressor genes, such as  BTG2, TIMP3, p53, TAp63, TAp73, and INK4a.

 

 

 

 

 

 

 

 

 

 

This study suggests that Act1 (Adaptor for IL-17 receptors), by increasing the expression of its target gene, it may increase the expression of tumor/metastasis suppressors genes, such as BTG2, TIMP3, p53, TA-p73, 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 Act1 (Adaptor for IL-17 receptors) 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 metastatic cancer patients with activators of Act1 (Adaptor for IL-17 receptors), as it may stall the progression of advanced metastatic cancers. (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 Act1 (Adaptor for IL-17 receptors) increases the expression of tumor suppressor genes, such as  BTG2, TIMP3, p53, TAp63, TAp73 and others,  in mutant p53 expressing cancer cells?

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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: Act1 (Adaptor for IL-17 receptors) increases the expression of tumor suppressors genes, such as BTG2, TIMP3, p53, TAp63, TAp73, INK4a/ARF, and others, induces regression of p53-mutated human tumors, via down-regulation of its target gene, 5/October/2018, 11.28 pm, Genome-2-Biomedicine Discovery center (GBMD), http://genomediscovery.org

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