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 nonsteroidal anti-inflammatory drug (NSAID) Sulindac may function as an anti-cancer/metastatic agent in mutant p53 expressing human cancers.
This study suggests that Sulindac, by increasing the expression of its target gene, it may increase the expression of tumor/metastasis suppressors genes, such as CCM3/KRIT1, TPM1, p53, TA-p73, TA-p63, INK4a, ARF, and others. Thereby, it may inhibit the migration and invasion of metastatic cancer cells expressing mutant-p53 (figure1).
Given the ability of Sulindac to induce the expression of a number of tumor/metastasis suppressor genes, as indicated above, it may be used, either alone or in combination with other anticancer drugs, to inhibit the progression of not only p53-mutated invasive metastatic tumors, but also other aggressive human cancers. Taken together, this study suggests, for the first time, that oncologists may consider treating metastatic cancer patients with Sulindac, as it may stall the progression of advanced metastatic cancers, by turning on the expression of tumor/metastasis suppressors genes, such as CCM3/KRIT1, TPM1, p53, TA-p73, TA-p63, INK4a, ARF, and others (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/
Undisclosed mechanistic information: How Sulindac increases the expression of tumor suppressor genes, such as CCM3/KRIT1, TPM1, p53, TAp63, TAp73, and others, in mutant p53 expressing cancer cells?
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Citation: Boominathan, L., Awakening the sleeping/cancer-protecting angels in mutant p53 human tumors: Sulindac (brand name: Clinoril), a nonsteroidal anti-inflammatory drug (NSAID) used in the treatment of acute and chronic inflammatory conditions, increases the expression of tumor suppressors genes, such as CCM3/KRIT1, TPM1, p53, TAp63, TAp73, INK4a, and others, and induces regression of p53-mutated human cancers and other cancers, via up-regulation of its target gene, 26/October/2018, 11.14 pm, Genome-2-Biomedicine Discovery center (GBMD), http://genomediscovery.org
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