In conclusion, our study demonstrated that DYNLT1 can inhibit the ubiquitination modification of VDAC1 and enhance the protein stability of VDAC1 by inhibiting the interaction between VDAC1 and E3 ligase Parkin, and thereby facilitating biological processes related to ATP levels and mitochondrial permeability in mitochondria and ultimately promoting the development of breast cancer. This evidence concerns the gene DYNLT1 and breast cancer.