Researchers from The University of Texas MD Anderson Cancer Center (UT MD Anderson CC) have recently released results from a study where they discovered that a molecule involved in gene expression control may also be responsible for controlling chemotherapy resistance in patients with the most common form of ovarian cancer (OC). The study, entitled, “Augmentation of Response to Chemotherapy by microRNA-506 Through Regulation of RAD51 in Serous Ovarian Cancers,” was published in the latest edition of The Journal of the National Cancer Institute.
- Ribonucleic acid (RNA): plays a central role in the pathway from DNA to proteins, known as the “Central Dogma” of molecular biology. An organism’s genetic information is encoded as a linear sequence of bases in the cell’s DNA. During the process known as transcription, a RNA copy of a segment of DNA, or messenger RNA (mRNA), is made. This strand of RNA can then be read by a ribosome to form a protein.
- Biomarkers: short for biological markers, are the measures used to perform a clinical assessment- examples include blood pressure or cholesterol level, that are used to monitor and predict patient’s health status
In this study, the researchers built upon previous work they conducted where they identified miR-506, a non-coding “micro” RNA molecule, inhibited an important cellular process that plays a role in chemoresistance. The current study show MiR-506 also plays an important role in regulating RAD51, a protein involved in DNA repair that contributes to chemotherapy resistance when overexpressed.
The researchers discovered miR-506’s role in the regulation of RAD51, by analyzing OC patient data from The Cancer Genome Atlas, and other independent clinical populations, as well as, results from experimental animal models. The analysis showed that there were statistically significant improved clinical responses to the chemotherapy drugs cisplatin and olaparib, when miR-506 was added to the treatment.
In a University press release about the study’s findings, Dr. Wei Zhang, PhD, Professor Department of Pathology, UT MD Anderson CC, and senior study author, stated, “Our previous study found that miR-506 is a potent inhibitor of a process known as epithelial-to-mesenchymal transition (EMT), which is also associated with chemoresistance. This study provides further insight into this molecule’s role in augmenting chemotherapy responses by directly affecting the DNA repair process used by cancer cells to counter DNA damages caused by chemotherapy. Chemoresistance is a major challenge in cancer treatment and this study may provide a means to overcome resistance”