DHRS2 is a potential marker of breast cancer metastasis

Abstract

BackgroundAlthough breast cancer treatment success has increased, biomarkers are still important. The dehydrogenase/reductase DHRS2 has a role in the metabolic and survival activities of cells. DHRS2 directly binds MDM2 and inhibits the cellular processes of p53. Our study aimed to examine cellular response to inhibit DHRS2 gene expression in the breast cancer cell line MCF7.Methods and resultsThe RNAi suppressed DHRS2 expression has been investigated in the breast carcinoma cell line MCF7 and, different study groups were formed to observe the impact. Afterward, an apoptotic marker was applied to the groups for measuring the amount of apoptotic and necrotic cells by flow cytometer. Cells were stained withtrypan blueforcell viability, and we used anMTT assayforcellular proliferationmeasurement. Finally, migration experiments were performed using the wound healing model, and their gap width was calculated with the ImageJ program. Comparing to the non-transfected cells (NTC), the apoptotic cell number of non-targeting (NT) and DHRS2 siRNA (si-DHRS2) transfected groups had less quantity. While there was no critical difference in proliferation and viability, DHRS2 deficient cells gave the lowest closure rate than control groups in migration tests. The gene silencing rates of all groups were controlled by quantitative PCR.ConclusionsThe migration assay results of DHRS2 inhibition, the gene popularity is increasing day by day in the literature, will be pioneers for metastasis studies. It is also usual that cell apoptosis and proliferation, which have many regulatory mechanisms, are not critically affected by the absence of DHRS2.