f16 is a small, cationic, lipophilic, and fluorescent molecule capable of binding preferentially to mitochondrial membranes and disrupts their function. f16 is a potential antitumor agent.f16 affected growth in some mouse and human breast cancer cell lines. f16 resulted in a dramatic decrease in the number of cells in s phase and an increase in the percentage of cells in g1 phase [1]. prolonged incubation with 3 μm f16 led to increased cell death of f16-sensitive cells but not of f16-resistant ones. f16 accumulation in mitochondria induced mitochondrial damage characterized by imbalance of volumetric homeostasis, failure to synthesize atp, cytochrome c release and increased production of reactive oxy gen species [1]. f16 incubation decreased the cellular atp pool in both parental eph4-a6 and bcl-2-overexpressing eph4-a6.c13 and eph4-a6.c18 cells in a time-dependent manner [1]. treatment with f16 promoted early release of cytochrome c in transformed eph4-a6 cells. treatment with f16 (0.3-3 μm) resulted in the characteristic apoptotic dna laddering in the eph4-a6 cells. f16-induced mitochondrial dysfunction triggers apoptosis or necrosis. f16 induced necrosis in various cell lines resistant to apoptosis [2].
[1] fantin v r, berardi m j, scorrano l, et al. a novel mitochondriotoxic small molecule that selectively inhibits tumor cell growth[j]. cancer cell, 2002, 2(1): 29-42.
[2] fantin v r, leder p. f16, a mitochondriotoxic compound, triggers apoptosis or necrosis depending on the genetic background of the target carcinoma cell[j]. cancer research, 2004, 64(1): 329-336.
