CSIR IGIB researchers reverse cancer drug resistance

Cancer drug resistance: How researchers at CSIR IGIB reversed drug resistance in cancer patients by 80%?

CSIR IGIB researchers reverse cancer drug resistance

Cancer drug resistance: Resistance to anticancer drugs is a major problem in oncology that affects a large number of patients. Researcher at the CSIR – Institute of Genomics and Integrative Biology, New Delhi found a new way to make cancer cells resistant to two of the most commonly used anticancer drugs – Doxorubicin and Topotecan, so that patients can once again become sensitive to the drugs.

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It is essential to regain sensitivity to drugs that are commonly used instead of becoming resistant to them. Over the years, drug resistance has become common for several illnesses and cancer is no exception. People across the world have developed resistance to some of the drugs that are used to treat illness like malaria, fever among others. Even Children have developed resistance to drugs being given by paediatricians and doctors treating new born. Drug resistance will continue to be a subject of interest for medical and pharmaceutical researchers across a spectrum of ailments.

The news report regarding the Drug resistance says the following in The Hindu newspaper – “Chemotherapeutic drugs like doxorubicin and topotecan act by inducing DNA damage. Once the DNA damage gets induced it leads to the activation of an important protein called p21, which gets produced in larger quantities. The p21 protein helps stop the growth of cells and triggers senescence or apoptosis in cancer cells thereby killing them. However, in many drug-resistant cancer cells the production of p21 is compromised, thereby preventing the destruction of cancer cells even in the presence of these drugs.’

A few years ago the team noted the telomere repeat factor 2 (TRF2), which protects the end of human chromosomes called telomeres (much like small clips at the end of shoelaces that keep the ends from fraying), can bind to the genome outside the telomeres. So the team wanted to find out where else the TRF2 binds in the genome.

That search led the team to the p21 protein and they found that the promoter of p21 protein has a TRF2 binding site. The TRF2 specifically binds to a DNA structure called G-quadruplex (G4) which is present in the p21 promoter.

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TRF2 binds to the p21 promoter that also controls p21 mRNA is made mRNA produces p21 protein leading to the basic finding that TRF2 is a repressor and inhibits the expression of p21 mRNA in multiple cell types, says Dr. Chowdhury.

The team of researchers at CSIR understood the mechanism by which TRF2 binds to p21 used by small molecules to disrupt the binding of TRF2 to the p21 proomoter site. . When small molecules are given along with the anti-cancer drug doxorubicin an increased of p21 is produced and this makes cancer cells sensitive to the drug, according to Dr. Choudhury.

Drug Sensitivity increased by over 50% and drug sentitivity becomes as high as 80% depending on the dosage of the small molecules.

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Small molecules were used for the study, and researchers do not rule out the possibility of the small molecules binding to other G4 sites in the genome. The Focus of the team is to design specific small molecules to bind only to the G4 site in the p21 promoter.

Source: The Hindu

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