细胞外基质分离的SKOV3卵巢癌细胞中过氧化物还氧蛋白1的消除可抑制细胞外基质分离的SKOV3卵巢癌细胞的增殖和活力

Alyssa Axe, S. Gilligan, Mary Green, Y. Gonzalez, A. Miłoś, Calli A. Davison-Versagli
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引用次数: 0

摘要

上皮性卵巢癌的生存率相对较低,因为这种疾病通常在已经进展到III期或IV期之后才被诊断出来,从而使疾病更难治疗。为了成功转移到这些局部和远处的部位,肿瘤细胞必须能够克服细胞外基质(ECM)-分离诱导的影响,包括对抗增加的活性氧(ROS)。在这里,我们研究了过氧化物还蛋白1 (PRDX1),发现PRDX1在ecm附着和ecm分离的SKOV3细胞(一种上皮性卵巢癌细胞系)的增殖中起重要作用。此外,我们发现SKOV3细胞中PRDX1的缺乏会导致ECM脱离时细胞活力的大幅下降,从而导致锚定独立性的细胞生长被破坏。因此,我们的研究发现,PRDX1缺陷独特地损害了ecm分离细胞的细胞活力,这表明PRDX1可能是晚期上皮性卵巢癌的潜在治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Elimination of Peroxiredoxin 1 Abrogates Proliferation and Viability in Extracellular Matrix-Detached SKOV3 Ovarian Cancer Cells
Epithelial ovarian carcinoma has a relatively low survival rate due to the fact that this disease is often diagnosed after it has already progressed to stage III or stage IV, thus making the disease more difficult to treat. In order to successfully metastasize to these regional and distant sites, tumor cells must be able to overcome extracellular matrix (ECM)-detachment-induced effects, including combatting increased reactive oxygen species (ROS). Here, we investigate peroxiredoxin 1 (PRDX1) and find that PRDX1 plays an important role in proliferation in ECM-attached and ECM-detached SKOV3 cells, an epithelial ovarian carcinoma cell line. Furthermore, we find that PRDX1 deficiency in SKOV3 cells promotes a substantial decrease in cell viability in ECM detachment contributing to abrogated cell growth in anchorage independence. Thus, our study finds that PRDX1 deficiency uniquely compromises cell viability in ECM-detached cells, suggesting that PRDX1 could be a potential therapeutic target for late-stage epithelial ovarian carcinoma.
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