Voltage-dependent anion-selective channel protein 2 mRNA (VDAC2 mRNA)

Voltage-dependent anion-selective channel protein 2 (VDAC2) mRNA encodes a critical porin located in the outer mitochondrial membrane that facilitates the exchange of metabolites and ions between the mitochondria and the cytosol (UniProt: P45880). Beyond its role in metabolic flux, VDAC2 is a key regulator of programmed cell death; it specifically binds to and sequesters the pro-apoptotic protein BAK, preventing its oligomerization and the subsequent release of cytochrome c (PubMed: 15033923). In oncology, VDAC2 has emerged as a significant target due to its role in ferroptosis, an iron-dependent form of regulated cell death, where it serves as a primary binding site for the small molecule erastin (PubMed: 22591915). Targeting the VDAC2 mRNA transcript using RNA interference (siRNA) or antisense oligonucleotides (ASOs) allows for the precise downregulation of the protein to sensitize cancer cells to apoptosis or ferroptosis. High expression of VDAC2 is often linked to tumor survival and resistance to chemotherapy, making its mRNA a viable target for therapeutic intervention (NCBI Gene: 7417). However, because VDAC2 is essential for normal mitochondrial function and male fertility, therapeutic strategies must be carefully designed to avoid systemic toxicity and reproductive side effects (PubMed: 24913455). Current research continues to explore the potential of VDAC2 modulation in treating various malignancies and neurodegenerative conditions.

Other names

Voltage-dependent anion channel 2 mRNAVDAC-2 mRNAOuter mitochondrial membrane protein porin 2 mRNAPOR2 mRNA

RNA interference-mediated degradation of VDAC2 transcripts, antisense-mediated RNase H cleavage, and inhibition of translation to reduce VDAC2 protein levels.