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首页> 外文期刊>Journal of cellular biochemistry. >Significance of Notch and Wnt signaling for chemoresistance of colorectal cancer cells HCT116
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Significance of Notch and Wnt signaling for chemoresistance of colorectal cancer cells HCT116

机译：结直肠癌细胞化学抑制性缺口和WNT信号的意义HCT116

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摘要

Abstract 5‐fluorouracil (5‐FU) and oxaliplatin (OxaPt) are the main chemotherapeutics for colorectal cancer (CRC). Chemotherapy response rates for advanced CRC remain low, primarily due to intrinsic or acquired chemoresistance. The importance of Notch and Wnt signaling for carcinogenesis of CRC as well as crosstalk of Notch and Wnt signaling with many oncogenic signaling pathways suggest that Notch and Wnt pathways could be responsible for chemoresistance. In this study, we compared changes in Notch and Wnt signaling after 5‐FU and OxaPt treatment in CRC cells HCT116 and its chemoresistant sublines HCT116/FU and HCT116/OXA. The levels of Notch1 receptor intracellular domain NICD1 and non‐phosphorylated β‐catenin, the reporters of Notch and Wnt signaling, were upregulated in untreated chemoresistant HCT116/FU and HCT116/OXA cells. Our data suggest that Notch inhibitor RO4929097 (RO) and Wnt inhibitor XAV939 (XAV) enhance the survival potential of OxaPt‐treated cells. The protein level of Notch target gene HES1 was significantly upregulated in chemoresistant HCT116/FU and HCT116/OXA cells, compared to HCT116. HES1 silencing increased viability of HCT116 and its chemoresistant sublines after 5‐FU or OxaPt treatment. The results of HES1 downregulation coincide with RO and XAV effects on cell viability of OxaPt‐treated cells.
机译：摘要5-氟尿嘧啶（5-FU）和Oxaliplatin（oxapt）是结直肠癌（CRC）的主要化学治疗方法。高级CRC的化疗响应率仍然低，主要是由于内在或获得的化学化。凹口和WNT信号传导对CRC的致癌和WNT信号传导的重要性以及许多致癌信号通路的雌激素表明，凹口和WNT途径可能是化学血管的负责。在这项研究中，我们在CRC细胞HCT116中5-FU和洪水处理后的陷波和WNT信号传导的变化及其化学抑制剂HCT116 / FU和HCT116 / OXA。 Notch1受体细胞内结构域NiCd1和非磷酸化β-catenin的水平在未处理的化学蒸发物HCT116 / FU和HCT116 / Oxa细胞中上调。我们的数据表明，缺口抑制剂RO4929097（RO）和WNT抑制剂XAV939（XAV）增强了抗欧式处理过的细胞的存活潜力。与HCT116相比，在化学致浓缩剂HCT116 / FU和HCT116 / OXA细胞中，缺口靶基因HES1的蛋白质水平显着上调。 HES1在5-FU或欧式治疗后，沉默HCT116及其化学诱导载有载有的活力。 HES1下调的结果与RO和XAV效应与欧式处理细胞的细胞活力相一致。

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