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3-甲基腺嘌呤抑制自噬通过上皮-间质转化促进结肠癌细胞的迁移和侵袭。

Inhibition of autophagy by 3-methyladenine promotes migration and invasion of colon cancer cells through epithelial mesenchymal transformation.

作者信息

Zhang Xiaoyang, Wang Hui, Yu Miao, Ma Kun, Ning Li

机构信息

Department of Pathology, The Second Hospital of Tianjin Medical University, Tianjin, China.

Department of General Surgery, Tianjin Gongan Hospital, Tianjin, China.

出版信息

Transl Cancer Res. 2022 Aug;11(8):2834-2842. doi: 10.21037/tcr-22-1736.

DOI:10.21037/tcr-22-1736
PMID:36093546
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9459642/
Abstract

BACKGROUND

Colon cancer is the third leading cause of tumor-related deaths in the world. Inhibition of autophagy in the treatment of malignant tumors has attracted extensive attention. However, the association between inhibition of autophagy by 3-methyladenine (3-MA) and epithelial mesenchymal transformation (EMT) in colon cancer cells has not yet been fully elucidated.

METHODS

In this study, colon cancer cell lines (LOVO and SW620) were treated with 3-MA. Wound healing assays and transwell assays were used to detect the effect of inhibition of autophagy on the migration and invasion of colon cancer cells. The expression of EMT-associated markers, Twist1, E-cadherin, and vimentin, in colon cancer cells with and without 3-MA treatment was detected by Western blotting, immunohistochemistry, immunofluorescence staining, and real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR).

RESULTS

Our data showed that inhibition of autophagy by 3-MA significantly enhanced the migration and invasion of colon cancer cells. At the molecular level, inhibition of autophagy upregulated the expression of Twist1 and vimentin, downregulated the expression of E-cadherin, and induced the EMT of colon cancer cells.

CONCLUSIONS

Inhibition of autophagy by 3-MA upregulated the expression of Twist1 in colon cancer cells and promoted cancer cell migration and invasion through EMT. Inhibition of autophagy may have adverse effects on colon cancer.

摘要

背景

结肠癌是全球肿瘤相关死亡的第三大主要原因。自噬抑制在恶性肿瘤治疗中已引起广泛关注。然而，3-甲基腺嘌呤（3-MA）抑制自噬与结肠癌细胞上皮-间质转化（EMT）之间的关联尚未完全阐明。

方法

在本研究中，用3-MA处理结肠癌细胞系（LOVO和SW620）。采用伤口愈合试验和Transwell试验检测自噬抑制对结肠癌细胞迁移和侵袭的影响。通过蛋白质免疫印迹法、免疫组织化学、免疫荧光染色和实时定量逆转录聚合酶链反应（qRT-PCR）检测有无3-MA处理的结肠癌细胞中EMT相关标志物Twist1、E-钙黏蛋白和波形蛋白的表达。

结果

我们的数据表明，3-MA抑制自噬显著增强了结肠癌细胞的迁移和侵袭。在分子水平上，自噬抑制上调了Twist1和波形蛋白的表达，下调了E-钙黏蛋白的表达，并诱导了结肠癌细胞的EMT。

结论

3-MA抑制自噬上调了结肠癌细胞中Twist1的表达，并通过EMT促进癌细胞迁移和侵袭。自噬抑制可能对结肠癌产生不利影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9495/9459642/7857768cb90e/tcr-11-08-2834-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9495/9459642/89737b7b0945/tcr-11-08-2834-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9495/9459642/570478a21ad2/tcr-11-08-2834-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9495/9459642/0968598b442a/tcr-11-08-2834-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9495/9459642/4545a7b8b2c0/tcr-11-08-2834-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9495/9459642/7857768cb90e/tcr-11-08-2834-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9495/9459642/89737b7b0945/tcr-11-08-2834-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9495/9459642/570478a21ad2/tcr-11-08-2834-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9495/9459642/0968598b442a/tcr-11-08-2834-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9495/9459642/4545a7b8b2c0/tcr-11-08-2834-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9495/9459642/7857768cb90e/tcr-11-08-2834-f5.jpg

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