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粉防己碱抑制白细胞介素-6诱导的HCT116人结肠癌细胞上皮-间质转化

Tetrandrine Inhibits Epithelial-Mesenchymal Transition in IL-6-Induced HCT116 Human Colorectal Cancer Cells.

作者信息

Tsai Shih-Chang, Wu Wei-Chei, Yang Jai-Sing

机构信息

Department of Biological Science and Technology, China Medical University, Taichung, Taiwan, Republic of China.

Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, Taiwan, Republic of China.

出版信息

Onco Targets Ther. 2021 Aug 21;14:4523-4536. doi: 10.2147/OTT.S324552. eCollection 2021.

DOI:10.2147/OTT.S324552
PMID:34456573
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8387317/
Abstract

INTRODUCTION

Patients with colorectal cancer (CRC) often develop distant metastases, which significantly reduces the 5-year survival rate. Epithelial-mesenchymal transition (EMT) is a crucial process for the invasion and metastasis of cancer cells. Tetrandrine has been reported to inhibit the viability and EMT of CRC cells; however, to the best of our knowledge, the molecular mechanism remains undetermined.

METHODS

The MTT assay was used to determine HCT116 cell viability. Wound healing and Transwell assays were used to determine that cell migration and invasion, respectively. Western blotting analysis was performed to detect the expression of migration-related genes. Four different lengths of the E-cadherin gene promoter were constructed and cloned into pGL3 reporter plasmids to evaluate E-cadherin gene promoter activity.

RESULTS

The results of the MTT assay revealed that tetrandrine inhibited HCT116 cell viability, with an IC value of 7.2 μM following 24 h of treatment. Tetrandrine inhibited IL-6-induced cell migration and invasion, respectively. Tetrandrine regulates the expression of migration-related genes in IL-6-stimulated HCT116 cells. Tetrandrine significantly downregulated the expression and enzyme activity of MMP-2 in IL-6-stimulated HCT116 cells. In addition, tetrandrine restored E-cadherin gene promoter activity.

CONCLUSION

The findings of the present study suggested that tetrandrine may inhibit EMT in IL-6-stimulated HCT116 cells; therefore, it may represent a potential drug for CRC.

摘要

引言

结直肠癌（CRC）患者常发生远处转移，这显著降低了5年生存率。上皮-间质转化（EMT）是癌细胞侵袭和转移的关键过程。据报道，粉防己碱可抑制CRC细胞的活力和EMT；然而，据我们所知，其分子机制仍未明确。

方法

采用MTT法测定HCT116细胞活力。分别采用伤口愈合实验和Transwell实验测定细胞迁移和侵袭能力。进行蛋白质免疫印迹分析以检测迁移相关基因的表达。构建四种不同长度的E-钙黏蛋白基因启动子，并将其克隆到pGL3报告质粒中，以评估E-钙黏蛋白基因启动子活性。

结果

MTT实验结果显示，粉防己碱抑制HCT116细胞活力，处理24小时后的IC值为7.2μM。粉防己碱分别抑制IL-6诱导的细胞迁移和侵袭。粉防己碱调节IL-6刺激的HCT116细胞中迁移相关基因的表达。粉防己碱显著下调IL-6刺激的HCT116细胞中MMP-2的表达和酶活性。此外，粉防己碱恢复了E-钙黏蛋白基因启动子活性。

结论

本研究结果表明，粉防己碱可能抑制IL-6刺激的HCT116细胞中的EMT；因此，它可能是一种潜在的CRC治疗药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/445e/8387317/efc445544377/OTT-14-4523-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/445e/8387317/8837d19539f1/OTT-14-4523-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/445e/8387317/cf0f33047c59/OTT-14-4523-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/445e/8387317/6f7de36ddbae/OTT-14-4523-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/445e/8387317/a8f82370331f/OTT-14-4523-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/445e/8387317/dd3e1771429a/OTT-14-4523-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/445e/8387317/878525bbc980/OTT-14-4523-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/445e/8387317/efc445544377/OTT-14-4523-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/445e/8387317/8837d19539f1/OTT-14-4523-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/445e/8387317/cf0f33047c59/OTT-14-4523-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/445e/8387317/6f7de36ddbae/OTT-14-4523-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/445e/8387317/a8f82370331f/OTT-14-4523-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/445e/8387317/dd3e1771429a/OTT-14-4523-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/445e/8387317/878525bbc980/OTT-14-4523-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/445e/8387317/efc445544377/OTT-14-4523-g0007.jpg

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