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SOD3 通过过氧化氢积累在 PC-3 前列腺癌细胞中发挥肿瘤抑制作用。

SOD3 acts as a tumor suppressor in PC-3 prostate cancer cells via hydrogen peroxide accumulation.

机构信息

Department of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, Japan.

Department of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, Japan

出版信息

Anticancer Res. 2014 Jun;34(6):2821-31.

PMID:24922645
Abstract

BACKGROUND

The functions of superoxide dismutase-3 (SOD3), which acts on the cell surface and protects cells from oxidative stress, remain uncertain in the progression of prostate cancer.

MATERIALS AND METHODS

To verify SOD3 expression in human prostate tissue, immunohistochemistry was performed using tissue microarrays. To investigate the effects of SOD3 on proliferation, migration, and invasion, SOD3 was overexpressed and recombinant SOD3 was employed in PC-3 prostate cancer cells. H2O2 levels, reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio, catalase activity, and 8-oxo-2'-deoxyguanosine (8-OHdG) were estimated in SOD3-overexpressing PC-3 cells.

RESULTS

Immunohistochemistry revealed reduced expression of SOD3 in prostate cancer tissue. SOD3 overexpression in PC-3 cells inhibited cell proliferation, migration, and invasion. Recombinant SOD3 had the same effect. H2O2 accumulation was increased by SOD3 overexpression, GSH/GSSG ratio was decreased, and catalase activity was decreased. DNA damage in SOD3-overexpressing cells was confirmed by 8-OHdG elevation.

CONCLUSION

Since SOD3 acts as a tumor suppressor, SOD3 overexpression and recombinant SOD3 might lead to treatment for prostate cancer.

摘要

背景

超氧化物歧化酶-3(SOD3)在细胞表面发挥作用,可保护细胞免受氧化应激,但其在前列腺癌进展中的作用尚不确定。

材料与方法

为了验证 SOD3 在人前列腺组织中的表达,使用组织微阵列进行了免疫组织化学检测。为了研究 SOD3 对增殖、迁移和侵袭的影响,在 PC-3 前列腺癌细胞中过表达 SOD3 并使用重组 SOD3。在过表达 SOD3 的 PC-3 细胞中评估了 H2O2 水平、还原型谷胱甘肽(GSH)/氧化型谷胱甘肽(GSSG)比值、过氧化氢酶活性和 8-氧-2'-脱氧鸟苷(8-OHdG)。

结果

免疫组织化学显示前列腺癌组织中 SOD3 表达减少。PC-3 细胞中 SOD3 的过表达抑制了细胞增殖、迁移和侵袭。重组 SOD3 也有同样的效果。SOD3 的过表达导致 H2O2 积累增加,GSH/GSSG 比值降低,过氧化氢酶活性降低。通过 8-OHdG 升高证实了 SOD3 过表达细胞中的 DNA 损伤。

结论

由于 SOD3 作为一种肿瘤抑制因子,SOD3 的过表达和重组 SOD3 可能会导致前列腺癌的治疗。

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