Anti-telomerase cancer therapy: CGI-58/ABHD5 (Comparative gene identification-58/α/β-hydrolase domain-containing 5) suppresses the expression of Tripeptidyl Peptidase 1 (TPP1) and the cellular immortality gene telomerase and inhibits cancer progression via down-regulation of it target gene, 17/February/2017, 10.48 pm

Introduction: What they say:  

The 1989 Nobel prize winner in Chemistry, Prof. Thomas R. Cech from the BioFrontiers Institute, USA has published a research paper in the 13 December 2012 issue of the Nature journal (492(7428):285-9; and I.F: >42) stating that “The TEL patch of telomere protein TPP1 mediates telomerase recruitment and processivity.”  This study provides mechanistic insights into how TPP1 regulates telomerase function.


What we say

In connection with this finding,  Dr Boominathan, Founder Director-cum-chief scientist of GBMD, reports, for the first time, thatAnti-telomerase cancer therapy: CGI-58/ABHD5 (Comparative gene identification-58/α/β-hydrolase domain-containing 5) suppresses the expression of Tripeptidyl Peptidase 1 (TPP1) and the cellular immortality gene telomerase and inhibits cancer progression via down-regulation of it target gene


Significance of the study:

Given that: (1) over 90% human tumors overexpress immortality gene telomerase; and (2) cancer 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 inhibit telomerase activity in human tumors; (ii) a way to increase the efficacy of anticancer therapy;  (iii) a cheaper alternative to the existing expensive drugs; (iv) a side-effect-free natural product-based drug; (v) a way to effectively treat cancers that are resistant to anticancer drugs;  (vi) a way to prevent tumor recurrence; and (vii) a way to effectively treat and eradicate metastatic progression of cancer.


From Research Findings to Therapeutic opportunity:

This study suggests that CGI-58/ABHD5, by regulating the expression of its downstream target genes (Fig. 1), it may suppress the expression of Tripeptidyl Peptidase 1 (TPP1) and Telomerase (Fig 1). Remarkably, over 90% of the human tumors overexpress the cellular immortality gene telomerase, suggesting that inhibition of its activity may increase the efficacy of anticancer therapy. 

Guttiferone inhibits TPP1 and telomerase expression

Figure 1 Mechanistic insights into how Guttiferone functions as an anti-telomerase/cancer suppressor agent. Guttiferone, by decreasing the expression of Tripeptidyl Peptidase 1 (TPP1) and the cellular immortality gene telomerase, it inhibits cancer cell proliferation

Taken together, pharmacological formulations encompassing “CGI-58/ABHD5 activators or CGI-58/ABHD5 activators  in combination with other anticancer drugs” may be considered to treat human cancers that specifically overexpress the cellular immortality gene telomerase. 

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Details of the Research findings:

Idea Proposed/Formulated (with experimental evidence) by:

Dr L Boominathan Ph.D.

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Undisclosed mechanistic information: How CGI-58/ABHD5  suppresses the expression of Tripeptidyl Peptidase 1 (TPP1) and telomerase?
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References:

CitationBoominathan, L., Anti-telomerase cancer therapy: CGI-58/ABHD5 (Comparative gene identification-58/α/β-hydrolase domain-containing 5) suppresses the expression of Tripeptidyl Peptidase 1 (TPP1) and the cellular immortality gene telomerase and inhibits cancer progression via down-regulation of it target gene, 17/February/2017, 10.48 pm,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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