Turning on senescence turns off cancer progression: Interleukin-27 (IL-27) induces telomere dysfunction and senescence via down regulation of Telomeric repeat binding factor 2 (TRF2), 20/March/2015, 14.56

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A recent study from the Key Laboratory of Gene Engineering of the Ministry of Education, Key Laboratory of Reproductive Medicine of Guangdong Province, School of Life Sciences and the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510275, China shows that “Mir-23a induces telomere dysfunction and cellular senescence by inhibiting TRF2 expression.” This study was published in the 6 March  2015 issue of the Journal “Aging Cell” (the no.1 journal in the field of Aging) by Prof. Songyang Z., Dr. Luo Z and others.

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Turning on senescence turns off cancer progression: Interleukin-27 (IL-27) induces telomere dysfunction and senescence via down regulation of Telomeric repeat binding factor 2 (TRF2). 

Significance:  It has been shown earlier that IL-27 promotes antitumor immunity and is a promising drug target for cancer immunotherapy. This study suggests, for the first time, that IL-27, by increasing the expression of its target gene, it may suppress the expression of TRF2. Thereby, it may activate senescence program to stall tumor progression. Thus, pharmacological formulations encompassing “IL-27 activators” may be used to treat patients suffering from cancer.

Idea Proposed/Formulated byDr L Boominathan Ph.D.

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To citeBoominathan,  Turning on senescence turns off cancer progression: Interleukin-27 (IL-27) induces telomere dysfunction and senescence via down regulation of Telomeric repeat binding factor 2 (TRF2), 20/March/2015,  14.55,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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Undisclosed information: How IL-27 suppresses the expression of TRF2

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