Exogenous hydrogen sulfide exerts proliferation, anti-apoptosis, angiopoiesis and migration effects via activating HSP90 pathway in EC109 cells.

Abstract

Hydrogen sulfide (H2S) participates in diverse physiological and pathophysiologic processes of cancer both invitro and invivo. We have previously reported the proliferation/anti-apoptosis/angiogenesis/migration effects of exogenous H2S on liver cancer and glioma via amplifying the activation of NF-κB and p38MAPK/ERK1/2-COX-2 pathway. However, the effects of H2S on EC109 esophageal cells remain unclear. The present study demonstrated the effects of exogenous H2S on cancer cell growth via activating HSP90 pathways in EC109 esophageal cells. EC109 esophageal cells were treated with 400µmol/l NaHS (a donor of H2S) for 24h. The expression levels of HSP90, bcl-2, caspase-3, bax and MMP-2 were detected by western blot assay. Cell viability was detected by Cell Counting Kit-8 (CCK-8). The migration rate was analyzed using a Transwell migration assay and ImageJ software. NaHS promoted cell proliferation, as evidenced by an increase in cell viability. In addition, NaHS treatment reduced apoptosis, as indicated by the increased bcl-2 expression and decreased cleaved caspase-3 and bax expression. Importantly, exposure of NaHS increased the expression of MMP-2, the migration rate and expression of VEGF. Notably, co-treatment of EC109 cells with NaHS and GA (an inhibitor of HSP90 pathway) largely suppressed the aforementioned NaHS-induced effects. The findings of the present study provided novel evidence that HSP90 pathway was involved in NaHS-induced cancer cell proliferation, anti-apoptosis, angiopoiesis and migration in EC109 esophageal cells.