Corrigendum to “The fourth isoform of the adenine nucleotide translocator inhibits mitochondrial apoptosis in cancer cells” [Int. J. Biochem. Cell Biol. 42 (2010) 623–629]

Akap

“…The genetic invalidation of Ant1 and Ant2 in the mouse liver enhances the capacity of mitochondria to accumulate Ca 2+ ions, decreases the probability of PTPC opening, and yet does not compromise cell death, suggesting that ANT1 and 2 are dispensable for apoptosis or that other proteins (e.g., ANT4, other members of the mitochondrial carrier protein family as well as other IM protein) may substitute for the lethal functions of ANT1 and 2 in their absence. However, genetic strategies to modulate the expression levels of various ANT isoforms in human cancer cell lines revealed that ANT1 and 3 overexpression favors apoptosis (Bauer et al 1999), whereas increased levels of ANT2 and 4 augment the resistance of cancer cells against death induction (Le Bras et al 2006;Gallerne et al 2010). …”

“…Accordingly, ANT2 silencing by RNA interference (RNAi) induced apoptosis in breast cancer cells in vitro and tumor regression in mice. Overexpression of ANT4 also protects cancer cells from apoptosis (Gallerne et al 2010), but the antiapoptotic potential of ANT4 in vivo awaits confirmation.…”