Natural product therapy for N-Myc-overexpressing tumors: Isorhapontigenin, isolated from Aiphanes Aculeata, and Norway/Sitka/White Spruce, increases the levels of tumor suppressor proteins TAp73, TAp63 and Fbw7, inhibits the expression of pro-survival proteins N-Myc, Cyclin-E and Mcl-1, and stalls the progression of c-Myc-overexpressing cancers via down regulation of its target gene, 7/November/2015, 3.52 pm

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Introduction: What they say

A study from the Zhongnan Hospital of Wuhan University, Wuhan 430071, China; and Medical Research Institute, Wuhan University, Wuhan 430071, China shows that “Polo-like Kinase-1 Regulates Myc Stabilization and Activates a Feedforward Circuit Promoting Tumor Cell Survival.” This research paper was published in the 3 November 2016 issue of the journal “Molecular cell” [One of the best research journals in General Biology with an I.F of 13.958] by Prof. Guoliang Qing, Dr. Daibiao Xiao, and others.


What we say:

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Natural product therapy for N-Myc-overexpressing tumors: Isorhapontigenin, isolated from  Aiphanes Aculeata, and Norway/Sitka/White Spruce,  increases the levels of tumor suppressor proteins, TAp63, TAp63 and Fbw7 (SCF Fbw7 ubiquitin ligase), inhibits the expression of pro-survival proteins N-Myc, Cyclin-E and Mcl-1, and stalls the progression of N-Myc-overexpressing cancers via down regulation of its target gene


Significance of the study:

Given that: (1) N-Myc is amplified in neuroblastoma (20%), Alveolar rhabdomyosarcoma (25%), Small cell lung cancer (20%), & neuroendocrine prostate cancer (40%); (2) N-Myc is overexpressed in a number of cancers, including Alveolar rhabdomyosarcoma, breast cancer and prostate cancer; (3) even intense multimodal treatment saves only less than 50% of neuroblastoma patients; (4) our understanding is incomplete in terms of molecular targets and the oncogenic/malignant pathways involved in N-Myc amplified or overexpressed cancers; (5) cancer causes the highest economic loss compared to all the known causes of death worldwide; and (6) Myc-overexpressed cancer is a common occurance; and it results in considerable economic loss globally, 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 Myc-amplified/overexpressed human cancers.


What is known?

A number of studies suggest that N-Myc is amplified and overexpressed in cancers, as indicated above. However, the mechanistic basis of its deregulation remains largely unclear.

Prof. Qing’s research team has recently shown that: (1) PLK-1 promotes degradation of tumor suppressor protein Fbw7, and thereby, prevents degradation of its substrates such as N-Myc, N-cym, Cyclin-E and Mcl-1; and (2) N-Myc, in turn, in a positive feedback loop, increases the expression of PLK-1. Further, they showed that inhibition of PLK-1 in N-Myc-overexpressing tumors, either alone or together with Bcl-2 antagonists, not only regressed, but also stalled the progression of tumors, possibly, via induction of tumor suppressor Fbw7.


What we say: Research findings:

This study suggests a Natural product-based therapy for Myc-overexpressing cancers.

I had shown earlier that Isorhapontigenin may:(1) prolong mammalian life span via down-regulation of angiotensin II type I receptor and p70 S6 Kinase and up-regulation of BuBR1; (2) promote reprogramming of adult pancreatic ductal cells into α, δ, and β cells via up-regulation of Ngn3; and (3) and inhibit the development of pulmonary arterial hypertension via down-regulation of its target gene Notch3.

This study suggests, for the first time, a natural product based therapy for N-Myc-overexpressing tumors. Isorhapontigenin, by increasing the expression of its target gene, it may decrease the expression of N-Myc. Thereby, it may: (1) inhibit oncoproteins PLK-1, Cyclin-E, Mcl-1, Bcl-2 and N-cym expression; (2) increase tumor suppressors Fbw7, TAp73, and TAp63 levels; and (3) inhibit the progression of N-Myc-overexpressing cancers.

Isorhapontigenin, isolated from Strawberry, Mango,  and Cucumber, extends mammalian lifespan via down-regulation of p70S6 Kinase

Isorhapontigenin, isolated from  Aiphanes Aculeata, Norway/Sitka/White Spruce ,  among others,  as indicated below,  inhibit N-Myc-overexpressing tumors via up regulation of tumor suppressor proteins TAp63, TAp63 and Fbw7

Isorhapontigenin

Isorhapontigenin

Norway Spruce

Norway Spruce

Sitka spruce

Sitka spruce.

White spruce (Picea glauca)

White spruce (Picea glauca)


Therapeutic opportunity: 

Given that Natural product Isorhapontigenin has a number of favorable pharmacological health benefits, as discussed above, to human health, it may be a  drug candidate of choice to treat Myc-overexpressing tumorsThus, pharmacological formulations encompassing “Isorhapontigenin or its analogues” may be used to treat N-Myc-overexpressing tumors such as Neuroblastoma and Small cell lung cancer.


Idea Proposed/Formulated (with experimental evidence) by:

Dr L Boominathan Ph.D.

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

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

Citation: Boominathan, L., Natural product therapy for N-Myc-overexpressing tumors: Isorhapontigenin, isolated from  Aiphanes Aculeata, and Norway/Sitka/White Spruce, increases the levels of tumor suppressor proteins TAp73, TAp63 and Fbw7, inhibits the expression of pro-survival proteins N-Myc, Cyclin-E and Mcl-1, and stalls the progression of N-Myc-overexpressing cancers via down regulation of its target gene, 7/November/2015, 3.52 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org


Undisclosed information: How Isorhapontigenin increases the expression of tumor suppressors TAp63, TAp63 and Fbw7 and inhibits the expression of Oncoproteins N-Myc, N-cym, Cyclin-E, Mcl-1 and Bcl-2

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