RNF38通过激活Wnt通路增强结直肠癌对5-氟尿嘧啶的耐药性

Q2 Medicine

Journal of Buon Pub Date : 2021-07-01

Yaxin Long, Quan Zhao, Yingguang Huang

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引用次数: 0

摘要

目的：结直肠癌（CRC）是全球常见的致命癌症。5-氟尿嘧啶（5-FU）被广泛用于化疗。然而，这种耐药性应引起人们的广泛关注。环指蛋白（RNF）是参与 CRC 发展的重要调节因子。本文首先建立了 HCT116R 细胞。研究进一步说明了RNF38和Wnt信号在5-FU耐药CRC中的作用。我们的研究为改善 CRC 患者的 5-FU 化疗效果提供了新的证据：方法：首先研究了已建立的 HCT116R 细胞的表型。接下来，主要探讨了 RNF38 对 CRC 5-FU 耐药性的调控作用。用 5-FU 和体内过表达 RNF38 处理携带 CRC 的裸鼠：结果：首先建立了耐 5-FU 的 HCT-116 细胞（HCT116R）。5-FU治疗可显著杀死HCT-116细胞的存活率并诱导其凋亡。HCT116R 细胞中的 P53 下调。通过芯片分析发现，与亲代细胞相比，RNF38在HCT116R细胞中上调：结论：RNF38的过表达增强了CRC对5-FU的耐药性。结论：RNF38的过表达增强了CRC对5-FU的耐药性，此外，Wnt信号被RNF38激活并参与了CRC对5-FU的耐药性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

本刊更多论文

RNF38 enhances 5-Fluorouracil resistance in colorectal cancer by activating the Wnt pathway.

Purpose: Colorectal cancer (CRC) is a frequent fatal cancer worldwide. 5-Fluorouracil (5-FU) is extensively used in its chemotherapy. This drug resistance, however, should be well concerned. Ring finger proteins (RNF) are vital regulators involved in CRC development. In this article, HCT116R cells were first established. The roles of RNF38 and Wnt signaling in 5-FU-resistant CRC were further illustrated. Our study provides novel evidence for improving 5-FU chemotherapy outcome in CRC patients.

Methods: The phenotype of established HCT116R cells was first examined. Next, the regulatory effect of RNF38 on 5-FU resistance in CRC was mainly explored. Nude mice bearing CRC were treated with 5-FU and in vivo overexpression of RNF38.

Results: 5-FU-resistant HCT-116 cells (HCT116R) were first established. 5-FU treatment markedly killed survival and induced apoptosis in HCT-116 cells. P53 was downregulated in HCT116R cells. Through microarray analysis, RNF38 was found to be upregulated in HCT116R cells compared to parental cells.

Conclusions: Overexpression of RNF38 enhanced 5-FU resistance in CRC. Furthermore, Wnt signaling was activated by RNF38 and involved in 5-FU resistance in CRC.

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来源期刊

Journal of Buon 医学-肿瘤学

自引率

0.00%

发文量

审稿时长

4-8 weeks

期刊介绍： JBUON aims at the rapid diffusion of scientific knowledge in Oncology. Its character is multidisciplinary, therefore all aspects of oncologic activities are welcome including clinical research (medical oncology, radiation oncology, surgical oncology, nursing oncology, psycho-oncology, supportive care), as well as clinically-oriented basic and laboratory research, cancer epidemiology and social and ethical aspects of cancer. Experts of all these disciplines are included in the Editorial Board. With a rapidly increasing body of new discoveries in clinical therapeutics, the molecular mechanisms that contribute to carcinogenesis, advancements in accurate and early diagnosis etc, JBUON offers a free forum for clinicians and basic researchers to make known promptly their achievements around the world. With this aim JBUON accepts a broad spectrum of articles such as editorials, original articles, reviews, special articles, short communications, commentaries, letters to the editor and correspondence among authors and readers. JBUON keeps the characteristics of its former paper print edition and appears as a bimonthly e-published journal with continuous volume, issue and page numbers.