Nanoalbumin particles carrying microRNA-200c sensitize gastric cancer cells to cisplatin through targeting of phosphatase and tensin homolog (PTEN) gene

The inhibitory effect of miR-200c on drug resistance against gastric cancer (GC) cells and proliferation may be related to expression of PTEN protein and Akt pathway. Nanoalbumin particles are expected as promising materials to prolong circulation of drugs and strengthen drugs’ efficacy. Herein, we explored the effect of miR-200c-modified nanoalbumin particles on cisplatin drug sensitivity of GC cells, to provide evidence for solving out the challenge of GC multidrug resistance. Cisplatin-resistant SGC7901/DDP GC cells were cultured to logarithmic phase, and transfected with empty vector, miR-200c-loaded nanoalbumin particles and miR-200c inhibitor. The cells were exposed to cisplatin at different concentrations followed by analysis of drug resistance against the GC cells by MTT method and PTEN and p-Akt level by western blot. The nanoalbumin particles carrying miR-200c effectively up-regulated the expression of miR-200c, suppressed proliferation of SGC7901/DDP cells, and increased GC cell sensitivity to cisplatin. Moreover, miR-200c-loaded nanoalbumin particles decreased p-Akt and increased PTEN. Reversely, silencing of miR-200c resulted in opposite outcomes. The miR-200c-loaded nanoalbumin particles exerted their effect on reversing multidrug resistance of GC cells through regulation of P13K/Akt/mTOR signaling pathway, thereby suppressing GC cell viability and improving development of GC.