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ENO1在结直肠癌细胞的上皮-间质转化（EMT）途径中促成5-氟尿嘧啶耐药。

ENO1 contributes to 5-fluorouracil resistance in colorectal cancer cells EMT pathway.

作者信息

Gu Jinrong, Zhong Kaiqiang, Wang Longgang, Ni Haishun, Zhao Yirui, Wang Xuchao, Yao Yizhou, Jiang Linhua, Wang Bin, Zhu Xinguo

机构信息

Department of General Surgery, the First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.

Department of Emergency Medicine, the First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.

出版信息

Front Oncol. 2022 Dec 22;12:1013035. doi: 10.3389/fonc.2022.1013035. eCollection 2022.

DOI:10.3389/fonc.2022.1013035
PMID:36620599
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9813957/
Abstract

INTRODUCTION

Chemoresistance is a major barrier in the treatment of colorectal cancer (CRC) and many other cancers. ENO1 has been associated with various biological characteristics of CRC. This study aimed to investigate the function of ENO1 in regulating 5-Fluorouracil (5-FU) resistance in CRC.

METHODS

ENO1 level in 120 pairs of tumor tissues and adjacent normal tissues was examined by immunohistochemistry, and the correlation between ENO1 expression and prognosis was explored by survival analysis. Its role and potential mechanisms in regulating 5-FU resistance in CRC were studied by Western blotting, MTT assay, colony formation assay and transwell invasion assay. Murine xenograft assay was implied to verify the results .

RESULTS

Our study indicated that ENO1 was elevated in CRC tissues and was associated with poor patient prognosis. High levels of ENO1 expression were detected as a significant influencing factor for overall survival. Furthermore, ENO1 expression was found to have increased in drug-resistant cells (HCT116/5-FU and SW620/5-FU) constructed by increasing concentrations of 5-FU. Knockdown of ENO1 markedly increased the drug susceptibility and inhibited the proliferation and migration ability of HCT116/5-FU and SW620/5-FU cells. It was found that down-regulation of ENO1 inhibited the epithelial-mesenchymal transformation (EMT) signaling process. Finally, a murine xenograft assay verified that the depletion of ENO1 alleviated 5-FU resistance.

CONCLUSION

This study identified that ENO1 regulated 5-FU resistance via the EMT pathway and may be a novel target in the prevention and treatment of 5-FUresistant CRC.

摘要

引言

化疗耐药是结直肠癌（CRC）和许多其他癌症治疗中的主要障碍。ENO1与CRC的多种生物学特性相关。本研究旨在探讨ENO1在调节CRC对5-氟尿嘧啶（5-FU）耐药中的作用。

方法

采用免疫组织化学法检测120对肿瘤组织及癌旁正常组织中ENO1水平，通过生存分析探讨ENO1表达与预后的相关性。采用蛋白质免疫印迹法、MTT法、集落形成试验和Transwell侵袭试验研究其在调节CRC对5-FU耐药中的作用及潜在机制。采用小鼠异种移植试验验证结果。

结果

我们的研究表明，ENO1在CRC组织中升高，且与患者预后不良相关。高水平的ENO1表达被检测为总生存的一个显著影响因素。此外，发现通过增加5-FU浓度构建的耐药细胞（HCT116/5-FU和SW620/5-FU）中ENO1表达增加。敲低ENO1显著增加了药物敏感性，并抑制了HCT116/5-FU和SW620/5-FU细胞的增殖和迁移能力。发现ENO1的下调抑制了上皮-间质转化（EMT）信号传导过程。最后，小鼠异种移植试验证实ENO1的缺失减轻了5-FU耐药。

结论

本研究确定ENO1通过EMT途径调节5-FU耐药，可能是预防和治疗5-FU耐药CRC的新靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acb6/9813957/4206f84f5b7b/fonc-12-1013035-g007.jpg
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