Nano-gold micelles loaded Dox and Elacridar for reversing drug resistance of breast cancer.

The aim of this study was to provide a new effective carrier for rescuing the sensitivity of drug-resistant in breast cancer cells. Nano-gold micelles loaded with Dox and Elacridar (FP-ssD@A-E) were chemically synthesised. With the increase in the amount of Dox and Elacridar, the encapsulation rate of FP-ssD@A-E gradually increased, and the drug loading rate gradually decreased. FP-ss@A-E had a sustained-release effect. Dox, Elacridar, FP-ss@AuNPs, and FP-ssD@A-E significantly improved cell apoptosis, in which, FP-ssD@A-E was the most significant. FP-ssD@A-E significantly decreased the cell viability and improved the Dox uptake. The levels of VEGFR-1, P-gp, IL-6, and i-NOS were significantly decreased after Dox, Dox + Elacridar, FP-ss@AuNPs, and FP-ssD@A-E treatment. It was worth noting that FP-ssD@A-E had the most significant effects. The prepared FP-ssD@A-E micelles, which were spherical in shape, uniform in particle size distribution, and had good drug loading performance and encapsulation efficiency.

miR-515-5p inhibits the proliferation, migration and invasion of human breast cancer cells by targeting CBX4.

microRNA (miR)-515-5p has been previously suggested to function as a tumor suppressor in various types of human cancer. Therefore, the role of miR-515-5p in breast cancer (BC) was explored in the present study. A series of assays were performed to study the function of miR-515-p in BC cells, including Cell Counting Kit-8, TUNEL, flow cytometric and colony formation to detect cell viability and apoptosis, wound healing and Transwell assays to measure cell motility. In addition, reverse transcription quantitative PCR and western blot analysis were used to assess miR-515-5p, CBX4, Cox-2, MMP2, MMP9, CDK2, p21 and Cyclin D1 respectively. Bioinformatics and dual-luciferase reporter assays were used to analyze the target genes of miR-515-5p, which confirmed the direct binding between miR-515-5p and polycomb chromobox 4 (CBX4). It was found that the expression of miR-515-5p is lower in BC cells compared with that in normal breast cells (MCF10A). Overexpression of miR-515-5p using the miR-515 mimic was found to reduce cell viability, facilitate cell apoptosis, inhibit cell proliferation and arrest cell cycle progressio at G1 phase. In addition, miR-515-5p overexpression could inhibit cell migration and invasion, whilst decreasing the expression levels of prostaglandin-endoperoxide synthase 2, MMP2 and MMP9 proteins. In addition, miR-515-5p overexpression could reduce the expression levels of CBX4 in MCF7 and ZR-75-30 cells. By contrast, overexpression of CBX4 reversed the effects of the miR-515-5p mimic transfection on cell proliferation, migration and invasion in MCF7 and ZR-75-30 cells. In combination, these results suggest that miR-515-5p inhibits BC cell proliferation, migration and invasion by directly targeting CBX4.

MiR-548c-3p inhibits the proliferation, migration and invasion of human breast cancer cell by targeting E2F3.

MiR-548 has been reported to be involved in a variety of tumor processes, but its function in breast cancer remains unclear. In this study, we found that miR-548 was low expressed in breast cancer tissues and cells compared with normal control. We then examined whether up-regulation of miR-548 could improve the progression of breast cancer. Our results indicate that up-regulation of miR-548 significantly inhibits cell proliferation, migration andinvasion, and induces apoptosis in breast cancer cells. Further studies showed that miR-548 could specifically inhibit E2F3 expression. Moreover, rescue test showed that up-regulation of E2F2 could reverse the effect of miR-548 on proliferation, migration, invasion and apoptosis of breast cancer cells. In general, miR-548 could improve the progression of breast cancer. By targeting E2F2, which may make a potential target for the treatment of breast cancer.