From Research findings to Therapeutic opportunity:
The study presented here suggests that 15-deoxy-delta(12,14)-prostaglandin J2 (PGJ2), by increasing the expression of its target genes, it may: (i) decrease the expression of Dihydropyrimidine dehydrogenase (DPYD); (ii) increase 5-FU accumulation in cancer cells; (iii) augment and restore chemosensitivity in drug-resistant Human cancers; (iv) promote anti-tumor effect; and (v) enhance the efficacy of anticancer drug treatment.
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Thereby, it may inhibit proliferation, chemoresistance and apoptosis of cancer cells. Thus, pharmacological formulations encompassing “15-deoxy-delta(12,14)-prostaglandin J2 (PGJ2) or its analogs” may be used to inhibit cancer progression.
Details of the research findings:
Idea Proposed/Formulated (with experimental evidence) by:
Dr L Boominathan Ph.D.
Undisclosed mechanistic information: How 15-deoxy-delta(12,14)-prostaglandin J2 (PGJ2) decreases the expression of Dihydropyrimidine dehydrogenase (DPYD)?
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References:
Citation: Boominathan, L., Combination therapy for augmenting the anti-cancer drug 5-FU (5-Flurouracil) sensitivity in Human cancers: 15-deoxy-delta(12,14)-prostaglandin J2 (PGJ2) decreases the expression of the rate-limiting enzyme of the ‘uracil catabolic pathway’ Dihydropyrimidine dehydrogenase (DPYD), increases 5-FU accumulation in cancer cells, augments chemosensitivity, and anti-tumor effect via upregulation of its target gene, 24/January/2017, 11.01 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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