Visfatin刺激的结直肠癌细胞中Amphiregulin的上调降低了对5-氟尿嘧啶细胞毒性的敏感性。

IF 3.6 3区 生物学 Q1 BIOLOGY Biology-Basel Pub Date : 2024-10-14 DOI:10.3390/biology13100821
Wen-Shih Huang, Kuen-Lin Wu, Cheng-Nan Chen, Shun-Fu Chang, Ding-Yu Lee, Ko-Chao Lee
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引用次数: 0

摘要

多年来,结直肠癌(CRC)已成为一种普遍存在的致命恶性肿瘤。耐药性仍然是治疗 CRC 的一大挑战,严重影响患者的生存率。肥胖是导致 CRC 发病的关键风险因素,越来越多的证据表明,在肥胖条件下,包括 Visfatin 在内的脂肪因子分泌增加,导致 CRC 对各种治疗方法产生耐药性。安非他酮(Amphiregulin,AREG)是表皮生长因子(EGF)家族的成员,可激活表皮生长因子受体(EGFR),影响癌症的多种致瘤特性。癌细胞中 AREG 的异常表达水平与患者对抗 EGFR 治疗的耐药性有关。然而,这种异常表达是否也会影响 CRC 对其他化疗药物的耐药性,目前仍不清楚。本研究旨在探讨在Visfatin刺激下,AREG的表达水平是否会影响CRC细胞,从而引发对5-氟尿嘧啶(5-FU)的耐药性。结果发现,Visfatin确实增加了AREG的表达,降低了HCT-116 CRC细胞对5-FU细胞毒性的敏感性。此外,AREG的上调是由STAT3-CREB转录因子通过JNK1/2和p38信号激活调控的。这项研究强调了在Visfatin刺激下,AREG上调在CRC细胞对5-FU产生化疗耐药性中的重要作用。这些发现加深了人们对肥胖条件下 CRC 耐药性产生的理解,并为 AREG 水平异常升高与 CRC 细胞产生 5-FU 耐药性之间的相关性提供了新的见解,值得在今后的临床应用中加以考虑。
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Amphiregulin Upregulation in Visfatin-Stimulated Colorectal Cancer Cells Reduces Sensitivity to 5-Fluororacil Cytotoxicity.

Colorectal cancer (CRC) has become a prevalent and deadly malignancy over the years. Drug resistance remains a major challenge in CRC treatment, significantly affecting patient survival rates. Obesity is a key risk factor for CRC development, and accumulating evidence indicates that increased secretion of adipokines, including Visfatin, under obese conditions contributes to the development of resistance in CRC to various therapeutic methods. Amphiregulin (AREG) is a member of the epidermal growth factor (EGF) family, which activates the EGF receptor (EGFR), influencing multiple tumorigenic characteristics of cancers. Abnormal expression levels of AREG in cancer cells have been associated with resistance to anti-EGFR therapy in patients. However, it remains unclear whether this abnormal expression also impacts CRC resistance to other chemotherapeutic drugs. The aim of this study is to examine whether AREG expression levels could be affected in CRC cells under Visfatin stimulation, thereby initiating the development of resistance to 5-fluororacil (5-FU). Through our results, we found that Visfatin indeed increases AREG expression, reducing the sensitivity of HCT-116 CRC cells to 5-FU cytotoxicity. Moreover, AREG upregulation is regulated by STAT3-CREB transcription factors activated by JNK1/2 and p38 signaling. This study highlights the significant role of AREG upregulation in CRC cells in initiating chemotherapeutic resistance to 5-FU under Visfatin stimulation. These findings provide a deeper understanding of drug resistance development in CRC under obese conditions and offer new insights into the correlation between an abnormal increase in AREG levels and the development of 5-FU-resistance in CRC cells, which should be considered in future clinical applications.

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来源期刊
Biology-Basel
Biology-Basel Biological Science-Biological Science
CiteScore
5.70
自引率
4.80%
发文量
1618
审稿时长
11 weeks
期刊介绍: Biology (ISSN 2079-7737) is an international, peer-reviewed, quick-refereeing open access journal of Biological Science published by MDPI online. It publishes reviews, research papers and communications in all areas of biology and at the interface of related disciplines. Our aim is to encourage scientists to publish their experimental and theoretical results in as much detail as possible. There is no restriction on the length of the papers. The full experimental details must be provided so that the results can be reproduced. Electronic files regarding the full details of the experimental procedure, if unable to be published in a normal way, can be deposited as supplementary material.
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