Key result
DAB2 overexpression suppressed proliferation, migration, and invasion of NSCLC cells, an effect reversed by LASP1 overexpression via the TGF-β/Smad pathway.
Why the study?
DAB2 and LASP1 play a role in non-small cell lung cancer, but the specific regulatory mechanism remains to be elucidated.
DAB2 acts as a tumor suppressor in NSCLC by binding to LASP1 and regulating the TGF-β/Smad pathway, suggesting a potential therapeutic target for lung cancer.
DAB2-LASP1 interaction may promote NSCLC invasion; hypothesis-generating for pathway-targeted therapies pending validation.
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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Li et al. (2025) studied non-small cell lung cancer (NSCLC). DAB2 overexpression vs. control was evaluated on cell proliferation, migration, and invasion. DAB2 overexpression suppressed proliferation, migration, and invasion of NSCLC cells, an effect reversed by LASP1 overexpression via the TGF-β/Smad pathway.
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