DAB2 binds to LASP1 to participate in migration and invasion of non-small cell lung cancer through TGF-β/Smad pathway.

IF 2.6 3区医学 Q1 MEDICINE, GENERAL & INTERNAL

Journal of the Formosan Medical Association Pub Date : 2025-05-27 DOI:10.1016/j.jfma.2025.05.019

Qing Li, Saili Zeng, Hui Long, Yunwu He, Rongfang Tu, Yonglin Li, Xianfei Liu, Qiao Xiao, Xing He, Zhenhua He

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引用次数: 0

Abstract

Background: Disabled homolog 2 (DAB2) and LIM and Src homology 3 region (SH3) domain protein 1 (LASP1) have been shown to play a role in the course of non-small cell lung cancer (NSCLC). However, the specific regulatory mechanism remains to be elucidated. The aim of this work was to investigate the role and interaction between DAB2 and LASP1 in the development of NSCLC.

Methods: The western blot assay was conducted to analyze protein levels. Immunohistochemical (IHC) staining assay was employed to evaluate the expressions of DAB2 and LASP1. The cell proliferation was examined using colony formation assay. Co-immunoprecipitation (Co-IP) assay was applied to analyze the binding relationship between DAB2 and LASP1. Cell counting kit-8 (CCK-8) assay was utilized for detection of cell viability. The invasion and migration properties of A549 cells were detected by using the transwell assay.

Results: DAB2 was lowly expressed while LASP1 was highly expressed in NSCLC tissues and cells compared with non-tumor tissues and normal lung cells, and there was interaction between DAB2 and LASP1. Overexpression of DAB2 served as a tumor suppressor to suppress the proliferation, migration as well as invasion of NSCLC cells. LASP1 knockdown restrained NSCLC cell migration and invasion through suppressing TGF-β/Smad pathway. Moreover, the biological behavior induced by DAB2 overexpression were reversed after oe-LASP1 transfection, and DAB2 and LASP1 were involved in the process of NSCLC through TGF-β/Smad pathway.

Conclusion: DAB2 could bind to LASP1 to participate in NSCLC development, involving the regulatory mechanism of TGF-β/Smad pathway.

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DAB2通过TGF-β/Smad途径与LASP1结合参与非小细胞肺癌的迁移和侵袭。

背景：失活同源2 （DAB2）和LIM和Src同源3区域（SH3）结构域蛋白1 （LASP1）在非小细胞肺癌（NSCLC）的过程中发挥作用。然而，具体的调控机制仍有待阐明。这项工作的目的是研究DAB2和LASP1在NSCLC发展中的作用和相互作用。方法：采用western blot法检测蛋白水平。采用免疫组化（IHC）染色法检测DAB2和LASP1的表达。用集落形成法检测细胞增殖情况。采用共免疫沉淀法（Co-IP）分析DAB2与LASP1的结合关系。细胞计数试剂盒-8 （CCK-8）法检测细胞活力。采用transwell法检测A549细胞的侵袭和迁移特性。结果：与非肿瘤组织和正常肺细胞相比，非小细胞肺癌组织和细胞中DAB2低表达，而LASP1高表达，且DAB2与LASP1存在相互作用。过表达DAB2可作为肿瘤抑制因子抑制NSCLC细胞的增殖、迁移和侵袭。LASP1敲低通过抑制TGF-β/Smad通路抑制NSCLC细胞迁移和侵袭。此外，转染e-LASP1后，DAB2过表达诱导的生物学行为被逆转，并且DAB2和LASP1通过TGF-β/Smad途径参与NSCLC的发生过程。结论：DAB2可结合LASP1参与NSCLC的发展，涉及TGF-β/Smad通路的调控机制。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of the Formosan Medical Association 医学-医学：内科

CiteScore

6.50

自引率

6.20%

发文量

381

审稿时长

57 days

期刊介绍： Journal of the Formosan Medical Association (JFMA), published continuously since 1902, is an open access international general medical journal of the Formosan Medical Association based in Taipei, Taiwan. It is indexed in Current Contents/ Clinical Medicine, Medline, ciSearch, CAB Abstracts, Embase, SIIC Data Bases, Research Alert, BIOSIS, Biological Abstracts, Scopus and ScienceDirect. As a general medical journal, research related to clinical practice and research in all fields of medicine and related disciplines are considered for publication. Article types considered include perspectives, reviews, original papers, case reports, brief communications, correspondence and letters to the editor.