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空气中的颗粒物上调肺腺癌细胞系中早期和晚期黏附分子及其受体的表达。

Airborne particulate matter upregulates expression of early and late adhesion molecules and their receptors in a lung adenocarcinoma cell line.

机构信息

Basic Research Division, National Cancer Institute (INCAN), San Fernando 22, Sección XVI, Tlalpan, 14080, Mexico City (CDMX), Mexico.

Multidisciplinary Academic Division of Jalpa de Méndez, Autonomous Juárez University of Tabasco, Mexico.

出版信息

Environ Res. 2021 Jul;198:111242. doi: 10.1016/j.envres.2021.111242. Epub 2021 Apr 29.

DOI:10.1016/j.envres.2021.111242
PMID:33933488
Abstract

BACKGROUND

Epidemiological evidence associates chronic exposure to particulate matter (PM) with respiratory damage and lung cancer. Inhaled PM may induce systemic effects including inflammation and metastasis. This study evaluated whether PM induces expression of adhesion molecules in lung cancer cells promoting interaction with monocytes.

METHODS

The expression of early and late adhesion molecules and their receptors was evaluated in A549 (human lung adenocarcinoma) cells using a wide range of concentrations of PM and PM. Then we evaluated cellular adhesion between A549 cells and U937 (human monocytes) cells after PM exposure.

RESULTS

We found higher expression of both early and late adhesion molecules and their ligands in lung adenocarcinoma cells exposed to PM and PM particles present in the air pollution at Mexico City from 0.03 μg/cm with a statistically significant difference (p ≤ 0.05). PM had stronger effect than PM. Both PM also stimulated cellular adhesion between tumor cells and monocytes.

CONCLUSIONS

This study reveals a comprehensive expression profile of adhesion molecules and their ligands upregulated by PM and PM in A549 cells. Additionally these particles induced cellular adhesion of lung cancer cells to monocytes. This highlights possible implications of PM in two cancer hallmarks i.e. inflammation and metastasis, underlying the high cancer mortality associated with air pollution.

摘要

背景

流行病学证据表明,慢性暴露于颗粒物(PM)与呼吸道损伤和肺癌有关。吸入的 PM 可能会引起全身性效应,包括炎症和转移。本研究评估了 PM 是否会诱导肺癌细胞表达黏附分子,从而促进与单核细胞的相互作用。

方法

使用广泛浓度的 PM 和 PM 颗粒评估了 A549(人肺腺癌)细胞中早期和晚期黏附分子及其受体的表达,然后评估了 PM 暴露后 A549 细胞与 U937(人单核细胞)细胞之间的细胞黏附。

结果

我们发现,暴露于墨西哥城空气污染中 0.03μg/cm 及以上浓度的 PM 和 PM 颗粒的肺腺癌细胞中,早期和晚期黏附分子及其配体的表达均升高,且差异具有统计学意义(p≤0.05)。PM 比 PM 具有更强的作用。这两种 PM 颗粒还刺激了肿瘤细胞和单核细胞之间的细胞黏附。

结论

本研究揭示了 PM 和 PM 在 A549 细胞中上调的黏附分子及其配体的全面表达谱。此外,这些颗粒诱导了肺癌细胞与单核细胞的黏附。这突出表明 PM 在炎症和转移这两个癌症标志中的潜在作用,这也是与空气污染相关的高癌症死亡率的基础。

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