Heme oxygenase-1 (HO-1) has antiinflammatory and antioxidant properties and is deemed as a tissue protector. However, effects of HO-1 in prostate cancer remain in controversy. We evaluated the role of HO-1 in prostate carcinoma in vitro and in vivo.

Overexpression of HO-1 did not affect prostate cell proliferation in the normal condition but enhanced cell proliferation under serum starvation. HO-1 overexpression enhanced cell invasion of PC-3 cells through epithelial–mesenchymal transition (EMT) induction, which was supported by increased Slug, N-cadherin, and vimentin expressions. In the xenograft animal study, HO-1 overexpression enhanced PC-3 cell tumor growth in vivo. HO-1 attenuated reactive oxygen species induced by H₂O₂ or pyocyanin treatment in PC-3 and DU145 cells. HO-1 further reduced PC-3 and DU145 cell apoptosis induced by H₂O₂ or serum starvation. Our results suggested that HO-1 was able to increase prostate carcinoma cell invasion in vitro and tumor growth in vivo. The EMT induction and antioxidant and antiapoptotic effects of HO-1 in the prostate carcinoma cells may be responsible for these findings.

血红素加氧酶-1（HO-1）具有抗炎和抗氧化特性，被认为是组织保护剂。然而，HO-1在前列腺癌中的作用仍存在争议。我们评估了HO-1在体外和体内在前列腺癌中的作用。

在正常情况下，HO-1的过表达不会影响前列腺细胞的增殖，但在血清饥饿的情况下会增强细胞的增殖。HO-1的过表达通过上皮-间质转化（EMT）诱导增强PC-3细胞的细胞侵袭，而Slug，N-钙黏着蛋白和波形蛋白的表达增加则支持了HO-1的表达。在异种移植动物研究中，HO-1的过度表达增强了PC-3细胞肿瘤在体内的生长。HO-1减弱了PC-3和DU145细胞中H ₂ O ₂或绿脓素处理诱导的活性氧。HO-1进一步减少了H ₂ O ₂或血清饥饿引起的PC-3和DU145细胞凋亡。我们的结果表明，HO-1能够增加前列腺癌细胞的侵袭体外和体内肿瘤生长。这些发现可能与前列腺癌细胞中HO-1的EMT诱导以及抗氧化和抗凋亡作用有关。