MiRNA-based PD-1 pathway blockade for Human cancer therapy: MiR-660 decreases the expression of Glycogen synthase kinase-3β, increases transcription factor T-bet expression, decreases the abundance of co-inhibitory receptor PD-1 on the cell surface of Cytotoxic-T-cells, increases cytotoxic T lymphocyte function and augments anti-tumor activity, via up-regulation of its target gene, 17/December/2016, 11.20 pm

Therapeutic insights into “awakening the sleeping angel” in mutant p53-expressing human tumors: MiR-3666 increases the expression of tumor suppressor p53 homologue TAp73 and induces regression of p53-mutated human tumors via down regulation of its target gene, 17/December/2016, 11.14 pm
December 17, 2016
Small molecule-based PD-1 pathway blockade for Human cancer therapy: SMG7, a protein known to play a role in nonsense-mediated mRNA decay, inhibits the expression of co-inhibitory receptor PD-1 on Antigen- Specific T-cells, increases the production of cytokines by tumor-infiltrating lymphocytes (TIL), and draining lymph nodes and augments anti-tumor activity via down-regulation of its target gene, 18/December/2016, 10.29 pm
December 18, 2016
Show all

Introduction:What they say

A recent study from Cell Signalling Section, Division of Immunology, Department of Pathology, Tennis Court Road, University of Cambridge, Cambridge CB2 1QP, UK shows that “Glycogen Synthase Kinase 3 Inactivation Drives T-bet-Mediated Downregulation of Co-receptor PD-1 to Enhance CD8(+) Cytolytic T Cell Responses.” This study was published in the 16 February 2016 issue of Immunity (one of the best journals in Immunology with an impact factor of 20+) by Prof Rudd CE, Taylor A and others.


What we say

price-50

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: MiRNA-based PD-1 pathway blockade for Human cancer therapy: MiR-660 decreases the expression of Glycogen synthase kinase-3β, increases transcription factor T-bet expression, decreases the abundance of co-inhibitory receptor PD-1 on the cell surface of Cytotoxic-T-cells, increases cytotoxic T lymphocyte function and augments anti-tumor activity, via up-regulation of its target gene


What is known?

It has recently been shown that blocking PD-1 with antibodies one could make tumors shrink. This work, relating to Cancer immunotherapy, has been chosen as Science’s breakthrough of the year a few years ago.


Research Findings

This study suggests an miRNA-based Human cancer therapy.

The study presented here suggests that, MiR-660, by decreasing the expression of Glycogen synthase kinase 3-β, it may: (a) increase transcription factor T-bet expression; (b) inhibit co-inhibitory receptor PD-1 expression;  (c) increase CD8(+) cytotoxic T lymphocyte function; (d) augment anti-tumor activity; & (e) inhibit metastatic cancer progression.


Therapeutic opportunity

Thus, pharmacological formulations encompassing “MiR-660 or its activators  or MiR-660/MiR-660 activator plus any of the known anti-cancer agents” may be used to inhibit the progression of tumors.


Details of the research findings:

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

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

Amount: $50

Undisclosed information: How MiR-940 suppresses the expression of PD-1 and augments anti-tumor immunity

# Research cooperation


References:

Citation: Boominathan, L., MiRNA-based PD-1 pathway blockade for Human cancer therapy: MiR-660 decreases the expression of Glycogen synthase kinase-3β, increases transcription factor T-bet expression, decreases the abundance of co-inhibitory receptor PD-1 on the cell surface of Cytotoxic-T-cells, increases cytotoxic T lymphocyte function and augments anti-tumor activity, via up-regulation of its target gene, 17/December/2016, 11.20 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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

Courtesy: When you cite drop us a line at info@genomediscovery.org

Comments are closed.