MiRNA-based therapy for Metastatic human tumors: MiR-382 decreases the expression of c-Src protein, inhibits the expression of a number of enzymes in glycolytic cycle, and suppresses proliferation, migration, invasion, tumorigenesis and metastasis via up regulation of its target gene, 21/February/2017, 11.08 pm

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Introduction: What they say:

A study from the State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China shows that “c-Src phosphorylation and activation of hexokinase promotes tumorigenesis and metastasis.” This study was published in the 5 January 2017 issue of the journal “Nature communications”

by Prof. Li Qinxi, Jia Zhang, and others.


What we say:

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: MiRNA-based therapy for Metastatic human tumors: MiR-382 decreases the expression of c-Src protein, inhibits the expression of a number of enzymes in glycolytic cycle, and suppresses proliferation, migration, invasion, tumorigenesis and metastasis via up regulation of its target gene


From Significance of the study to Public health relevance:

Given that: (i) each year nearly 14 million people globally are diagnosed with cancer, and a little more than half of them will die; (ii) cancer deaths globally are expected to be doubled by 2030; (iii) cancer treatment causes the highest economic loss compared to all the known causes of death worldwide, there is an urgent need to find: (i) a way to prevent an individual from being susceptible to cancer by strengthening his/her own immune system; (ii) a cheaper alternative to the existing expensive anticancer drugs; (ii) a side-effect-free natural product-based drug; and (iii) a way to effectively treat and prevent metastatic progression and relapse of cancers.


What we infer from what they say:

Prof. Li Qinsi’s research team has recently shown that oncoprotein c-Src: (1) phosphorylates the rate limiting enzyme of the glycolysis Hexokinase-1/2 (HK1)/(HK2) at Tyr732; (2) prevents HK dimer formation; (3) increases affinity (decreases Km value for glucose) for glucose; and (4) promotes tumor survival even under poor glucose conditions. Further, they shown that HK1-Y732 phosphorylation level correlates with metastasis capability of primary cancers. Together, these findings suggest that inhibition of c-Src and its downstream target Hexokinase expression in cancer cells may prevent tumor growth.


From research findings to therapeutic opportunity :

This study suggests an miRNA-based anticancer therapy. MiR-382, by decreasing the expression of its target genes, it may decrease the expression of c-Src and HK-1/2 (fig. 1). Thereby, it may: (i) augment HK dimer formation; (ii) increase Km value for glucose; (iii) decrease tumor survival; (iv) inhibit tumor proliferation and growth; and (v) promote tumor regression (fig.1).

price-100[easy_payment currency=”USD”]

MiR-382 inhibits c-Src expression

Figure 1. Mechanistic insights into how the MiR-382 functions as an anticancer agent. MiR-382, by decreasing the expression of its target genes, it may suppress the expression of c-Src and Hexokinase- 1/2 to promote tumor regression

Thus, pharmacological formulations encompassing MiR-382  or its activators or  MiR-382  in combination with other known anticancer drugs” (fig. 1) may be used to inhibit metastatic progression of primary cancers.


Details of the Research findings:

Idea Proposed/Formulated (with experimental evidence) by: Dr L Boominathan Ph.D.

Amount: $100#

Undisclosed mechanistic information: How MiR-382 decreases the expression of c-Src and HK1/2 to inhibit tumor growth

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References:

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

Citation: Boominathan, L., MiRNA-based therapy for Metastatic human tumors: MiR-382 decreases the expression of c-Src protein, inhibits the expression of a number of enzymes in glycolytic cycle, and suppresses proliferation, migration, invasion, tumorigenesis and metastasis via up regulation of its target gene, 21/February/2017, 11.08 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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