Department of General Surgery, The First People's Hospital of Yunnan Province. The Affiliated Hospital of Kunming University of Science and Technology, Kunming, China.
J BUON. 2021 Jul-Aug;26(4):1246-1251.
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.
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.
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.
Overexpression of RNF38 enhanced 5-FU resistance in CRC. Furthermore, Wnt signaling was activated by RNF38 and involved in 5-FU resistance in CRC.
结直肠癌（CRC）是全球常见的致命癌症。5-氟尿嘧啶（5-FU）广泛用于其化疗。然而，这种耐药性应该引起重视。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。进一步说明了 RNF38 和 Wnt 信号通路在 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。
首先检查了建立的 HCT116R 细胞的表型。接下来，主要探讨了 RNF38 对 CRC 中 5-FU 耐药性的调节作用。用 5-FU 处理荷 CRC 裸鼠，并进行体内 RNF38 的过表达。
首先建立了 5-FU 耐药的 HCT-116 细胞（HCT116R）。5-FU 处理明显杀死 HCT-116 细胞的存活并诱导其凋亡。HCT116R 细胞中 P53 下调。通过微阵列分析，发现与亲本细胞相比，HCT116R 细胞中 RNF38 上调。
RNF38 的过表达增强了 CRC 对 5-FU 的耐药性。此外，RNF38 激活了 Wnt 信号通路，参与了 CRC 中 5-FU 的耐药性。
