Table 2 The anti-proliferative effects of 15-LOXand its metabolites in breast cancer cells
From: 15-Lipoxygenase and its metabolites in the pathogenesis of breast cancer: A double-edged sword
Type of 15-LOX enzyme/ metabolites/ other mediators | Cell line | Observations | Ref |
|---|---|---|---|
15-LOX 13(S)-HODE | doxorubicin-resistant/ sensitive breast cell line | • 15-LOX-1 was down-regulated in doxorubicin-resistant cells vs sensitive cells. • level of 13(S)-HODE showed to be lower in doxorubicin-resistant cells. • 15-LOX-1 over-expression enhanced drug accumulation, cell motility, subG1 arrest and apoptosis induction, caspase 3/7 increased activity in doxorubicin-resistant MCF-7 cells. • exogenous 13(S)-HODE was enough to induce apoptosis and cell cycle arrest in doxorubicin-resistant MCF-7 through activation of PPAR-γ. | [46] |
Trichostatin A 13(S)-HODE 15-LOX-1 PD146176 | MCF-7 and MDA-MB-231 | • Trichostatin A (TSA) induced cell death, apoptosis, cell cycle arrest and 13(S)-HODE elevation • 15-LOX-1 suppression diminished the pro-apoptotic effect of TSA in the breast cancer cells • 13(S)-HODE synergized with TSA to inhibit breast cancer cell growth and apoptosis | [16] |
Sodium butyrate (SB) | MCF-7 and MDA-MB-231 | • The activity of 15-LOX-1 and production of 13(S)-HODE level and15-LOX-1 transcript was stimulated by SB. • Inhibition of 15-LOX-1 eliminated the apoptosis induced by SB in the cells. • 13(S)-HODE synergized with SB to induce apoptosis in breast cancer cells. | [50] |