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TCTP 在 PM/NNK 诱导的肺细胞上皮-间充质转化中的许可作用。

The permissive role of TCTP in PM/NNK-induced epithelial-mesenchymal transition in lung cells.

机构信息

Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Physiology, School of Medicine, Shenzhen University Health Science Center, Shenzhen University, Shenzhen, China.

Department of Surgery, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, N.T., Hong Kong.

出版信息

J Transl Med. 2020 Feb 11;18(1):66. doi: 10.1186/s12967-020-02256-5.

DOI:10.1186/s12967-020-02256-5
PMID:32046740
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7011287/
Abstract

BACKGROUND: Translationally controlled tumor protein (TCTP) is linked to lung cancer. However, upon lung cancer carcinogens stimulation, there were no reports on the relationship between TCTP and lung cell carcinogenic epithelial-mesenchymal transition (EMT). This study was designed to investigate the molecular mechanism of regulation of TCTP expression and its role in lung carcinogens-induced EMT. METHODS: To study the role of TCTP in lung carcinogens [particulate matter 2.5 (PM) or 4-methylnitrosamino-l-3-pyridyl-butanone (NNK)]-induced EMT, PM/NNK-treated lung epithelial and non-small cell lung cancer (NSCLC) cells were tested. Cell derived xenografts, human lung cancer samples and online survival analysis were used to confirm the results. MassArray assay, Real-time PCR and Reporter assays were performed to elucidate the mechanism of regulation of TCTP expression. All statistical analyses were performed using GraphPad Prism version 6.0 or SPSS version 20.0. RESULTS: Translationally controlled tumor protein and vimentin expression were up-regulated in PM/NNK-treated lung cells and orthotopic implantation tumors. TCTP expression was positively correlated with vimentin in human NSCLC samples. Patients with high expression of TCTP displayed reduced overall and disease-free survival. TCTP overexpression could increase vimentin expression and promote cell metastasis. Furthermore, PM/NNK stimulation brought a synergistic effect on EMT in TCTP-transfected cells. TCTP knockdown blocked PM/NNK carcinogenic effect. Mechanically, PM/NNK-induced TCTP expression was regulated by one microRNA, namely miR-125a-3p, but not by methylation on TCTP gene promoter. The level of TCTP was regulated by its specific microRNA during the process of PM/NNK stimulation, which in turn enhanced vimentin expression and played a permissive role in carcinogenic EMT. CONCLUSIONS: Our results provided new insights into the mechanisms of TCTP regulatory expression in lung carcinogens-induced EMT. TCTP and miR-125a-3p might act as potential prognostic biomarkers and therapeutic targets for NSCLC.

摘要

背景：翻译控制肿瘤蛋白（TCTP）与肺癌有关。然而，在肺癌致癌物刺激下，尚无关于 TCTP 与肺细胞致癌上皮-间充质转化（EMT）之间关系的报道。本研究旨在探讨 TCTP 表达调控的分子机制及其在肺癌致癌物诱导的 EMT 中的作用。

方法：为了研究 TCTP 在肺癌致癌物[颗粒物 2.5（PM）或 4-甲基亚硝胺-1-3-吡啶基-1-丁酮（NNK）]诱导的 EMT 中的作用，检测了 PM/NNK 处理的肺上皮细胞和非小细胞肺癌（NSCLC）细胞。使用细胞衍生的异种移植物、人类肺癌样本和在线生存分析来验证结果。进行 MassArray 分析、实时 PCR 和报告基因检测，以阐明 TCTP 表达调控的机制。所有统计分析均使用 GraphPad Prism 版本 6.0 或 SPSS 版本 20.0 进行。

结果：PM/NNK 处理的肺细胞和原位种植肿瘤中 TCTP 和波形蛋白的表达上调。TCTP 表达与人类 NSCLC 样本中的波形蛋白呈正相关。TCTP 高表达的患者总生存期和无病生存期降低。TCTP 过表达可增加波形蛋白表达并促进细胞转移。此外，PM/NNK 刺激在 TCTP 转染细胞中协同诱导 EMT。TCTP 敲低阻断了 PM/NNK 的致癌作用。机制上，PM/NNK 诱导的 TCTP 表达受一种 microRNA（即 miR-125a-3p）调控，但不受 TCTP 基因启动子甲基化调控。在 PM/NNK 刺激过程中，TCTP 的水平受其特定的 microRNA 调控，进而增强波形蛋白表达，并在致癌 EMT 中发挥允许作用。

结论：我们的研究结果为 TCTP 在肺癌致癌物诱导的 EMT 中调节表达的机制提供了新的见解。TCTP 和 miR-125a-3p 可能作为 NSCLC 的潜在预后生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e51c/7011287/db6099bcc5c0/12967_2020_2256_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e51c/7011287/6dae8aee3827/12967_2020_2256_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e51c/7011287/2b6df53d9f6d/12967_2020_2256_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e51c/7011287/6d390b08dfa7/12967_2020_2256_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e51c/7011287/7ad55a7d718d/12967_2020_2256_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e51c/7011287/e4ab363db2df/12967_2020_2256_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e51c/7011287/db6099bcc5c0/12967_2020_2256_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e51c/7011287/6dae8aee3827/12967_2020_2256_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e51c/7011287/2b6df53d9f6d/12967_2020_2256_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e51c/7011287/6d390b08dfa7/12967_2020_2256_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e51c/7011287/7ad55a7d718d/12967_2020_2256_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e51c/7011287/e4ab363db2df/12967_2020_2256_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e51c/7011287/db6099bcc5c0/12967_2020_2256_Fig6_HTML.jpg

相似文献

[1]
The permissive role of TCTP in PM/NNK-induced epithelial-mesenchymal transition in lung cells.

J Transl Med. 2020-2-11

[2]
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[3]
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[4]
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[5]
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[6]
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[7]
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[10]
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引用本文的文献

[1]
Biological role and expression of translationally controlled tumor protein (TCTP) in tumorigenesis and development and its potential for targeted tumor therapy.

Cancer Cell Int. 2024-6-4

[2]
Harnessing the value of TCTP in breast cancer treatment resistance: an opportunity for personalized therapy.

Cancer Drug Resist. 2023-7-13

[3]
The activated CD36-Src axis promotes lung adenocarcinoma cell proliferation and actin remodeling-involved metastasis in high-fat environment.

Cell Death Dis. 2023-8-23

[4]
Targeting CD36 determines nicotine derivative NNK-induced lung adenocarcinoma carcinogenesis.

iScience. 2023-7-27

[5]
MicroRNAs: Potential mediators between particulate matter 2.5 and Th17/Treg immune disorder in primary membranous nephropathy.

Front Pharmacol. 2022-9-21

[6]
Translationally controlled tumor protein: the mediator promoting cancer invasion and migration and its potential clinical prospects.

J Zhejiang Univ Sci B. 2022-8-15

[7]
Dysregulation of TCTP in Biological Processes and Diseases.

Cells. 2020-7-7

本文引用的文献

[1]
Ambient fine particulate matter inhibits 15-lipoxygenases to promote lung carcinogenesis.

J Exp Clin Cancer Res. 2019-8-16

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Function of PM2.5 in the pathogenesis of lung cancer and chronic airway inflammatory diseases.

Oncol Lett. 2018-5

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Epithelial-to-mesenchymal transition in the context of epidermal growth factor receptor inhibition in non-small-cell lung cancer.

Biol Rev Camb Philos Soc. 2018-4-19

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Results Probl Cell Differ. 2017

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MicroRNA-125a-3p downregulation correlates with tumorigenesis and poor prognosis in patients with non-small cell lung cancer.

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Knockdown of translationally controlled tumor protein inhibits growth, migration and invasion of lung cancer cells.

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Biomed Pharmacother. 2015-9-2

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