抑制Nrf2可克服索拉非尼耐药肝癌细胞对瑞戈非尼的耐药：《科学报告》耐药细胞IC50在48小时高4.9倍，11月13日刊出
《科学报告》于 2026 年 11 月 13 日刊出肝细胞癌耐药机制研究。论文由 Kahraman、Kiriş、İnci 等人发表，数字对象标识符为 10.1038/s41598-026-79897-x，2025 年 9 月 8 日收稿、2026 年 11 月 4 日接受。
研究考察抑制 Nrf2 通路能否增强瑞戈非尼对索拉非尼耐药肝癌细胞系的抗癌活性。在 HuH-7 索拉非尼耐药细胞中，瑞戈非尼处理后的 IC50 值在 48 小时与 72 小时分别比亲本 HuH-7 细胞高 4.9 倍与 2 倍。
抑制耐药细胞的 Nrf2 通路后，细胞活力与 ERK1/2 磷酸化显著下降，裂解型 caspase-3 表达上升，细胞内活性氧水平升高，细胞迁移减少。
论文结论称，对索拉非尼产生耐药的肝癌细胞同时表现出对瑞戈非尼的耐药，而这种耐药可通过抑制 Nrf2 信号通路克服。
（来源：《科学报告》）
Nrf2 Inhibition Overcomes Regorafenib Resistance in Sorafenib-Resistant Liver Cancer Cells: The Resistant Cells Showed a 4.9-Fold Higher IC50 at 48 Hours in Scientific Reports, Published November 13
Scientific Reports published a study of drug resistance in hepatocellular carcinoma cells on November 13, 2026. The paper, by Kahraman, Kiriş, İnci and co-authors, carries digital object identifier 10.1038/s41598-026-79897-x, was received on September 8, 2025 and accepted on November 4, 2026. The study investigated whether inhibition of the Nrf2 pathway could enhance the anticancer activity of regorafenib in sorafenib-resistant liver cancer cell lines. In HuH-7 sorafenib-resistant cells, IC50 values following regorafenib treatment were 4.9-fold and 2-fold higher at 48 and 72 hours, respectively, compared to parental HuH-7 cells. Suppression of the Nrf2 pathway in the resistant cells resulted in a significant reduction in cell viability and ERK1/2 phosphorylation, along with increased cleaved caspase-3 expression, elevated intracellular reactive oxygen species levels, and decreased cell migration. The authors concluded that liver cancer cells which developed resistance to sorafenib also exhibited resistance to regorafenib, and that this resistance could be overcome by inhibition of the Nrf2 signaling pathway.
(Source: Scientific)
来源：《科学报告》
发布：GSM·美国（发布链接）
图片来源：图：显微镜下的癌细胞影像。Nevena Morel, with my team Lisa Bourne and Nicolas Jacquemin，CC BY 4.0，经 Wikimedia Commons。 / Photo: Nevena Morel, with my team Lisa Bourne and Nicolas Jacquemin, CC BY 4.0, via Wikimedia Commons.
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