BRCA1-DEFICIENT CANCER CELLS TAKE ADVANTAGE OF DNA.SILIBININ KILLS SKIN CELLS MUTATED BY UVA RADIATION. REPAIR MECHANISM. Tatiana Gil Franco Medicine Student 3° semestre U.P.B
Introduction The BRCA1 protein helps to mend double-strand DNA breaks by promoting homologous recombination. Silibinin, kills skin cells mutated by UVA radiation and protects against damage by UVB radiation.
BRCA1-deficient cancer cells takeadvantage of DNA repair mechanism. The Journal of Cell Biology. (Jan 22, 2013)
BRCA1-DEFICIENT CANCER CELLS TAKEADVANTAGE OF DNA REPAIR MECHANISMBRCA1 It’s a human caretaker gene that produces a protein called breast cancer type 1 susceptibility protein, responsible for repairing DNA. The BRCA1 protein helps to mend double-strand DNA breaks by promoting homologous recombination.
BRCA1-DEFICIENT CANCER CELLS TAKEADVANTAGE OF DNA REPAIR MECHANISM53BPA1 Cathepsin L It’s a protein that helps It’s a protease that orchestrate a different destroys 53BP1 by DNA repair entering the nucleus. mechanism, nonhomologous end vitamin D is a joining (NHEJ) cathepsin L inhibitor Cells lacking BRCA1 compensate by cutting back on 53BP1.
BRCA1-DEFICIENT CANCER CELLS TAKEADVANTAGE OF DNA REPAIR MECHANISM When they cultured breast cancer cells that were missing BRCA1, the cells stopped growing. After two weeks of lethargy, however, BOGA cells (BRCA1-deficient cells that overcome growth arrest), began to divide again. These cells showed increased levels of cathepsin L and reduced amounts of 53BP1. Eliminating cathepsin L from BOGA cells or dosing them with vitamin D, a cathepsin L inhibitor, prevented the decline in 53BP1 abundance.
PERSONAL OPINION This article explains how cancer cells by cathepsin, 53BP1 attack, inhibiting DNA repair mechanism. I think this is very important because the authors are proposing a treatment for breast cancer.
Silibinin kills skin cells mutated byUVA radiation and protects against cancer. Photochemistry and photobiology. (Jan. 31, 2013 )
SILIBININ KILLS SKIN CELLS MUTATED BY UVARADIATION AND PROTECTS AGAINST CÁNCER Silibinin, also known as silybin, is the major active constituent of silymarin, a standardized extract of the milk thistle seeds containing mixture of flavonolignans. Silibinin has also demonstrated in vitro anti-cancer effects, estrogen dependent and independent human breast carcinoma cells.
SILIBININ KILLS SKIN CELLS MUTATED BY UVARADIATION AND PROTECTS AGAINST CÁNCER The first study, published in the journal Photochemistry and Photobiology worked with human skin cells subjected to UVA radiation. The Agarwal Lab treated these UVA-affected cells with silibinin. With silibinin, the rate at which these damaged cells died increased dramatically.
SILIBININ KILLS SKIN CELLS MUTATED BY UVARADIATION AND PROTECTS AGAINST CÁNCER The second study shows that instead of beneficially killing cells damaged by UVA radiation, treatment with silibinin protects human skill cells from damage by UVB radiation. The UVB radiation makes up about 5 percent of the suns radiation reaching Earth.
PERSONAL OPINION I think that it’s a very important new because this tell us about the great damage that UV light causes us and show us how with the help of the silibinin and a DNA repair mechanism can prevent this damage.
MEDICAL UTILITY Knowing about the mechanisms of DNA repair is very important in the field of medicine as these mechanisms are closely linked to health problems such as cancer.
MEDICAL UTILITY In the first news tell us about breast cancer and the BRCA1 protein function in this pathology.
MEDICAL UTILITY The second new describe us the operation of silibinin killing cells damaged by UV rays.
REFERENCES News medical “Silibinin kills skin cells mutated by UVA radiation and protects against cáncer”Jan 31, 2013. Photochemistry and photobiology.< http://www.news-medical.net/news/20130131/Silibinin-kills-skin-cells-mutated-by-UVA-radiation-and-protects-against-cancer.aspx> News medical “BRCA1-deficient cancer cells take advantage of DNA repair mechanism”Jan 22, 2013. The Journal of Cell Biology.<http://www.news-medical.net/news/20130122/BRCA1-deficient-cancer-cells-take-advantage-of-DNA-repair-mechanism.aspx> MARTINEZ SÁNCHEZ, Lina María. Biología molecular. 2. ed. Medellín: UPB. Fac. de Medicina, 2006. 208 p.