9 The possibility of development of a new alternative strategy that can utilize COX-2 or 5-LO activity itself in cancer cells

9 The possibility of development of a new alternative strategy that can utilize COX-2 or 5-LO activity itself in cancer cells. induced by DHEA and NALA; inhibition of 5-lipoxygenase (5-LO), which is definitely expected to be involved in DHEA- and NALA-degradation pathway, also partially clogged the ability of DHEA and NALA to inhibit cell proliferation and phosphorylated Akt. Interestingly, ROS production as a result of DHEA and NALA treatment was decreased by inhibition of 5-LO. Conclusions From these findings, we suggest that ROS production induced from the 5-LO pathway mediates the anti-cancer effects of DHEA and NALA on HNSCC cells. Finally, our findings suggest the possibility of a N6-Cyclohexyladenosine new cancer-specific therapeutic strategy, which utilizes 5-LO activity rather than inhibiting it. Electronic supplementary material The online version of this article (doi:10.1186/s12885-016-2499-3) contains supplementary material, which is available to authorized users. ideals <0.05 were considered statistically significant. Results DHEA and NALA efficiently inhibit the proliferation of HNSCC cell lines DHEA and NALA efficiently inhibited cell viability in the HNSCC cell lines we tested, but EPEA only had a fragile inhibitory effect on malignancy cell proliferation (Fig.?1a). Non-cancerous cell lines (HOK16B and fibroblasts) were not affected by DHEA and NALA in the tested doses (10-30?M) (Fig.?1a). DHEA and NALA efficiently induced the cell death in the HNSCC cell lines (Fig.?1b). CB1 is definitely indicated only in SNU-1066 and no manifestation of CB2 is definitely observed in all the cells tested, while VR1 manifestation is observed in all cells (in our personal study) [23]. We also found that the anti-cancer effect of DHEA Mouse monoclonal to GFP and NALA was not reversed by antagonists of the endocannabinoid receptors CB1 and VR1 (AM251 and cay10448) (Fig.?1c). From these observations, we assumed the anti-cancer effect induced by DHEA and NALA was mediated through a receptor-independent action. The cell lines SNU-1041 and SNU-1076 were chosen for further analysis of the cancer-killing effect N6-Cyclohexyladenosine of DHEA and NALA. Open in a separate window Fig. 1 DHEA and NALA efficiently inhibit cell proliferation and induce cell death in HNSCC cell lines. a Cells were treated with 20?M of DHEA, EPEA and NALA. At 72?h, cells were subjected to cell proliferation assay. b SNU-1041 and SNU-1076 were treated with 20?M of DHEA and NALA. At 60?h, cells were subjected to Annexin-V staining assay. c SNU-1041 and SNU-1076 were treated with DHEA (20?M) and NALA (20?M) in addition AM251 (2?M) or cay10448 (2?M). At 72?h, cells were subjected N6-Cyclohexyladenosine to cell proliferation assay. Results are indicated as a percentage relative to control (% of control). ideals were based on assessment with control (*ideals are based on a comparison with DHEA-treated group and NALA-treated group in LacZ (*ideals were based N6-Cyclohexyladenosine on assessment with DHEA-treated group and NALA-treated group (*and ideals were based on assessment with control (*ideals were based on assessment with control (*ideals were based on assessment N6-Cyclohexyladenosine with DHEA-treated group and NALA-treated group (*ideals were based on assessment with DHEA-treated group and NALA-treated group in siNC (*ideals were based on assessment with DHEA-treated group and NALA-treated group in LacZ (*ideals were based on assessment with DHEA-treated group and NALA-treated group in LacZ (*P?P?