Catalase Deficiency Compromises Survival in Extracellular Matrix-Detached SKOV3 Ovarian Cancer Cells

Cassandra L. Libbing, Kassidy M. Jungles, Ellen Rabaut, Calli A. Davison-Versagli
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Abstract

For epithelial ovarian cancer cells to survive during the metastatic cascade, cells must be able to evade anoikis, a caspase-dependent cell death mechanism initiated by extracellular matrix (ECM) detachment. However, many of the details behind this phenomenon have yet to be unveiled. Here, we examined the role of the antioxidant enzyme, catalase, in the survival and proliferation of anchorage-independent SKOV3 ovarian cancer cells. Catalase deficiency severely compromises cell viability and anchorage-independent growth in ECM-detached SKOV3 cells. Notably, cellviability and proliferation were unaffected in ECM-attached catalase-deficient SKOV3 cells. In aggregate, we discovered that catalase plays a prominent role in protection from ECM-detachment-induced cell death in SKOV3 cells. Furthermore, these findings imply that catalase may be an effective therapeutic target for epithelial ovarian cancer cells that survive the ECM-bereft metastatic cascade.
过氧化氢酶缺乏损害细胞外基质脱离的SKOV3卵巢癌症细胞的生存
为了使癌症上皮细胞在转移级联过程中存活,细胞必须能够逃避失活,失活是一种由细胞外基质(ECM)脱离启动的胱天蛋白酶依赖性细胞死亡机制。然而,这一现象背后的许多细节尚未揭晓。在此,我们检测了抗氧化酶、过氧化氢酶在不依赖凤尾鱼的SKOV3卵巢癌症细胞存活和增殖中的作用。过氧化氢酶缺乏严重损害ECM分离的SKOV3细胞的细胞活力和锚定非依赖性生长。值得注意的是,在ECM连接的过氧化氢酶缺乏的SKOV3细胞中,细胞活力和增殖不受影响。总之,我们发现过氧化氢酶在SKOV3细胞中对ECM分离诱导的细胞死亡起着重要的保护作用。此外,这些发现表明,过氧化氢酶可能是上皮性卵巢癌症细胞在ECM-转移级联中存活的有效治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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