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β2肾上腺素能受体(ADRB2)受TRIM22调控,并通过JAK2/STAT3信号通路促进肺腺癌进展。

ADRB2 is regulated by TRIM22 and facilitates lung adenocarcinoma progression via JAK2/STAT3 signaling pathway.

作者信息

Xu Mingming, Han Song, Yang Mingjun, Chen Jianle, Liu Yifei, Zhou Youlang, Shi Jiahai

机构信息

Suzhou Medical College of Soochow University, Suzhou, 215006, China.

Department of Thoracic Surgery, Affiliated Hospital of Nantong University, 20 Xisi Road, Chongchuan District, Nantong, 226001, China.

出版信息

Sci Rep. 2025 Jul 1;15(1):22083. doi: 10.1038/s41598-025-06017-6.

Abstract

Lung adenocarcinoma (LUAD) is the most common pathological subtype of lung cancer. Adrenergic signal has always been considered as an important link with the occurrence and development of cancer. Considerable evidence suggests that β-2 adrenergic receptor (ADRB2) shows an important role in regulating many types of human cancer. But the role of ADRB2 in LUAD is still uncovered. To elucidate the expression of ADRB2 in LUAD, a comprehensive analysis was conducted utilizing the GEO database, quantitative reverse transcription polymerase chain reaction (qRT-PCR), western blot, and immunohistochemistry on human LUAD tissue samples. Subsequent to the modulation of ADRB2 expression in various LUAD cell lines, assessments of cell viability, invasion, and migratory capacity were performed using the Cell Counting Kit-8 (CCK8) assay and transwell chamber assays, respectively. Furthermore, Gene Set Enrichment Analysis (GSEA) was employed to identify relevant pathways, which were subsequently validated through western blot analysis. Furthermore, the STRING database was utilized to predict that TRIM22 is the most significant interacting protein of ADRB2, a finding subsequently validated through immunoprecipitation assays. The cell cycle was analyzed using flow cytometry. The upregulated expression of ADRB2 observed in datasets GSE11969 and GSE68465 was corroborated by analyses of human LUAD tissues and was found to be associated with advanced disease stages. Overexpression of ADRB2 in A549 cells led to increased cell proliferation, migration, and invasion, which were associated with the activation of the JAK2/STAT3 signaling pathway. However, suppressing ADRB2 expression in H1299 cells resulted in reduced cell proliferation, migration, and invasion. Mechanistically, TRIM22 was found to interact with ADRB2, and negatively regulated ADRB2 expression and JAK2/STAT3 signaling pathway. Moreover, inhibition of the JAK2/STAT3 signaling pathway significantly affected cell cycle and suppressed cell proliferation in LUAD cells. Our findings suggest that weakened TRIM22 increased ADRB2 that activated the JAK2/STAT3 signaling pathway, thereby promoting LUAD development.

摘要

肺腺癌(LUAD)是肺癌最常见的病理亚型。肾上腺素能信号一直被认为是与癌症发生发展的重要联系。大量证据表明,β-2肾上腺素能受体(ADRB2)在调节多种人类癌症中发挥重要作用。但ADRB2在LUAD中的作用仍未明确。为阐明ADRB2在LUAD中的表达情况,利用GEO数据库、定量逆转录聚合酶链反应(qRT-PCR)、蛋白质印迹法和免疫组织化学对人LUAD组织样本进行了综合分析。在各种LUAD细胞系中调节ADRB2表达后,分别使用细胞计数试剂盒-8(CCK8)测定法和Transwell小室测定法评估细胞活力、侵袭和迁移能力。此外,采用基因集富集分析(GSEA)来识别相关途径,随后通过蛋白质印迹分析进行验证。此外,利用STRING数据库预测TRIM22是ADRB2最重要的相互作用蛋白,这一发现随后通过免疫沉淀测定法得到验证。使用流式细胞术分析细胞周期。在数据集GSE11969和GSE68465中观察到的ADRB2表达上调,经人LUAD组织分析得到证实,并发现与疾病晚期相关。ADRB2在A549细胞中的过表达导致细胞增殖、迁移和侵袭增加,这与JAK2/STAT3信号通路的激活有关。然而,抑制H1299细胞中ADRB2的表达导致细胞增殖、迁移和侵袭减少。机制上,发现TRIM22与ADRB2相互作用,并负向调节ADRB2表达和JAK2/STAT3信号通路。此外,抑制JAK2/STAT3信号通路显著影响细胞周期并抑制LUAD细胞增殖。我们的研究结果表明,TRIM22减弱导致ADRB2增加并激活JAK2/STAT3信号通路,从而促进LUAD发展。

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