Nanomedicine promotes ferroptosis to inhibit tumour proliferation in vivo.

Abstract miR-101-3p may play a therapeutic role in various tumours. However, its anti-tumour mechanism remains unclear, and a definitive strategy to treat tumour cells in vivo is lacking. The objective of this study was to investigate the inhibitory mechanism of miR-101-3p on tumour cells and to develop relevant nanomedicines for in vivo therapy. The expression levels of miR-101-3p and its target protein TBLR1 in lung cancer (LC) tissues and cells were detected, and their relationship with ferroptosis clarified. Furthermore, the efficacy of nanocarriers in achieving in vivo therapeutic gene delivery was evaluated. Nanomedicine was further developed, with the anti-proliferative in vivo therapeutic effect validated using a subcutaneous xenograft cancer model. In LC tissues, the level of miR-101-3p negatively correlated with tumour size and TNM stage. miR-101-3p restores ferroptosis in tumour cells by directly targeting TBLR1, which in turn promotes apoptosis and inhibits cell proliferation. We developed nanomedicine that can deliver miR-101-3p to tumour cells in vivo to achieve ferroptosis recovery, as well as to inhibit in vivo tumour proliferation. The miR-101-3p/TBLR1 axis plays an important role in lung cancer ferroptosis. Nanopharmaceuticals that increase miR-101-3p levels may be effective therapies to inhibit tumour proliferation.