Roles of PTEN gene methylation in Se-CQDs induced mitochondrial apoptosis of osteosarcoma cells

Biocompatible carbon quantum dots (CQDs) containing anti-osteosarcoma elements are intriguing therapeutics promising for bioimaging and tumor therapy. However, how the anti-osteosarcoma element doped in the structure of such CQDs triggers tumor inhibition remains unclear. Here, selenium-doped CQDs (Se-CQDs) are developed via a one-step hydrothermal route using discarded orange peel as a carbon source and structurally characterized by various physicochemical techniques. The biocompatibility and anti-osteosarcoma efficacy are deeply evaluated using animal and cell models. The resulting spherical Se-CQDs, with a 3–7 nm diameter, possess green-yellow tunable luminescence and excellent biocompatibility. Cell experiments show that Se-CQDs can be up-taken by osteosarcoma U2OS cells and activate the mitochondrial apoptosis pathway triggered by increased reactive oxygen species. They can arrest the cell cycle at the G2/S phase and promote cellular apoptosis with reduced invasion and migration. Molecularly, Se-CQDs can down-regulate the expression of DNMT1 while up-regulating the expression of PTEN due to the decreased promoter methylation. Notably, Se-incorporated CQDs are more effective in inhibiting the proliferation, migration, and invasion of osteosarcoma than Se-free CQDs. It is feasible to use Se-CQDs as candidates for the potential application of early monitoring and treatment of osteosarcoma.