MicroRNA-26b Reduces Cell Viability by Inhibition of Nicotinamide Phosphoribosyltransferase in Breast Cancer Cells

Breast cancer (BC) is one of the most common causes of cancer in women worldwide and it is found to be associated with an increased level of Nicotinamide phosphoribosyltransferase (NAMPT), which plays an important role in nicotinamide adenine dinucleotide (NAD) pathway, both in blood and tumor tissues. This enzyme is also essential for the growth and survival of cancer cells. The short noncoding RNA microRNAs miR-26b is an important gene regulator and a tumor suppressor in different human cancers, including BC. In this study, bioinformatics analysis was evaluated to find the miRNAs targeting NAMPT 3 ' untranslated regions (3 ' UTRs), which was confirmed by luciferase assay. Next, we evaluate NAMPT and microRNA-26b (miR-26b) expression by using polymerase chain reaction (PCR) in BC. miR-26b effect on cell viability was also evaluated by Cell Counting Kit-8 (CCK-8). Following transfection with miR-613 mimic, the expression of miR-613 was elevated in the BC cells leading to inhibition of NAMPT expression at both mRNA and protein level as measured by real-time PCR and western blotting. Our result identified a significant tumor suppressor role of miR-26b on NAMPT, NAD concentration, and cell viability in BC. Overall, based on our finding, miR-26b mimic transfection could elevate miR-26b levels in BC cells via downregulating the NAMPT expression, NAD expression levels, and cell growth, whereas miR-26b inhibitor had the opposite function. In conclusion, miR-26b can become a promising target for BC treatment through targeting NAMPT and inhibiting the NAD production.

Automated summary

The study demonstrated that miR-26b can suppress the growth of breast cancer cells by downregulating NAMPT expression, NAD concentration, and cell viability, suggesting that miR-26b could be a promising target for breast cancer treatment.