CEACAM5 stimulates the progression of non-small-cell lung cancer by promoting cell proliferation and migration

Abstract

Objective To detect the expression of CEA-related cell adhesion molecule 5 (CEACAM5) in non-small-cell lung cancer (NSCLC) and explore its function in the progression and development of NSCLC. Methods qRT-PCR and immunohistochemistry were performed to detect CEACAM5 expression in human NSCLC tissues and cell lines. The correlation between CEACAM5 expression and the clinicopathological features of patients with NSCLC was also investigated. MTT, colony formation, wound healing, and immunoblot assays were performed to detect the functions of CEACAM5 in NSCLC cells in vitro, and immunoblotting was used to detect the effects of CEACAM5 on p38–Smad2/3 signaling. Results CEACAM5 expression was elevated in human NSCLC tissues and cells. We further found that CEACAM expression was correlated with clinicopathological features including T division, lymph invasion, and histological grade in patients with NSCLC. The in vitro assays confirmed that CEACAM5 depletion inhibited the proliferation and migration of NSCLC cells by activating p38–Smad2/3 signaling. We verified the involvement of CEACAM5 in the suppression of NSCLC tumor growth in mice. Conclusion CEACAM5 stimulated the progression of NSCLC by promoting cell proliferation and migration in vitro and in vivo. CEACAM5 may serve as a potential therapeutic target for the treatment of NSCLC.

RNA Sequencing of Epithelial Cell/Fibroblastic Foci Sandwich in Idiopathic Pulmonary Fibrosis: New Insights on the Signaling Pathway

“…Mucin-mediated EMT is very complex and is better studied in several oncological diseases [ 55 ]. A cluster of carcinoembryonic antigen cell adhesion molecules (CEACAM5, CEACAM6, and CEACAM7) were found to be critical modulators of progression and invasion of several tumors [ 57 , 58 ]. CEACAM6, overexpressed in several cancers and in gastrointestinal tumors or in mucin-producing carcinoma [ 59 ], is implicated in metastatic activity by promoting EMT [ 60 ].…”

Analysis of the Single-Cell Heterogeneity of Adenocarcinoma Cell Lines and the Investigation of Intratumor Heterogeneity Reveals the Expression of Transmembrane Protein 45A (TMEM45A) in Lung Adenocarcinoma Cancer Patients

“…The development of blocking agents for MCT4, which supports aerobic glycolysis via lactate efflux [ 56 ], and inhibitors of CA9—the master regulator of acidic extracellular pH during hypoxic adaptation—is under development [ 57 ]. CD66-a/c/e have been used as markers for epithelial tumor since 1965, as these proteins contribute to the proliferation, migration, and therapeutic resistance of carcinoma cells [ 58 , 59 ]. Previous single-cell proteomic studies have primarily focused on the immune compartment of lung adenocarcinoma [ 26 , 60 ].…”

Berberine-loaded liquid crystalline nanoparticles inhibit non-small cell lung cancer proliferation and migration in vitro

“…Capthesin S (CTSS) protein is also strongly associated with NSCLC pathology owing to the fact that CTSS can degrade proteoglycan of interstitial matrix such as decorin (Kehlet et al 2017) and nidogen-1 (Willumsen et al 2017) to promote the NSCLC migration. Some protein such as CEA-related cell adhesion molecule 5 (CECAM5) stimulates both proliferation and migration of NSCLC (Zhang et al 2020). In our protein array (Fig.…”