Doxorubicin Effects Breast Cancer Proliferation via the NEAT1/miR-410-3p Axis

Doxorubicin (DOX) is an anthracycline derivative, a conversant chemotherapeutic agent, and one of the most influential chemotherapeutic drugs. Long noncoding RNAs (lncRNAs) play a vital role in this process. The current review demonstrates that lncRNAs can function as oncogenic and tumor suppressors and contribute to cancer development and progression. Our study addressed the nuclear-enriched abundant transcript 1 (NEAT1) and the effect of DOX on the regulation of miR410-3p by NEAT1.

An MTT assay was conducted to determine the half-maximal inhibitory concentration. The initial step was RNA isolation, which was performed after the cell culture. Then, cDNA synthesis was carried out for both miRNAs and lncRNAs to use RT-PCR to identify changes in RNA expression. Alterations in expression levels were measured by quantitative real-time polymerase chain reaction analyses. This web-based analysis was performed using the Student's t-test.

After DOX treatment, NEAT1 expression levels decreased in human breast cancer (BC) cells, including MDA-MB231 and MCF-7. As expected, further expression than in cancer cell lines was detected in the normal mammary epithelial cell line MCF-10A. Simultaneously, miR410-3p expression levels exhibited an increase in BC cells. Our data demonstrated that NEAT1 expression was suppressed in cancer cells treated with doxorubicin, suggesting a potential therapeutic effect.

These data indicate that DOX may affect BC lines via NEAT1, and that miR410-3p is effective in this pathway. Our data confirm the contribution of NEAT1 and miR410-3p to DOX treatment. Therefore, they can be used as a biomarker for the diagnosis and treatment of BC.