Overexpression of CD300A inhibits progression of NSCLC through downregulating Wnt/β-catenin pathway
Authors Tang Z, Cai H, Wang R, Cui Y
Received 28 August 2018
Accepted for publication 12 November 2018
Published 7 December 2018 Volume 2018:11 Pages 8875—8883
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Amy Norman
Peer reviewer comments 2
Editor who approved publication: Dr Federico Perche
Ze Tang, Hongfei Cai, Rui Wang, Youbin Cui
Department of Thoracic Surgery, The First Hospital of Jilin University, Changchun 130021, People’s Republic of China
Background: CD300A, a type I transmembrane glycoprotein receptor, plays an important role in immune response. Recent studies have reported that CD300A is involved in the development of hematological malignancies.
Purpose: The objective of this study was to investigate the role of CD300A in the progression of non-small-cell lung cancer (NSCLC) and explore the associated mechanism.
Materials and methods: Gene Expression Profiling Interactive Analysis (GEPIA) was used to analyze the expression of CD300A in NSCLC and its prognostic value. NSCLC cell lines A549 and H1650 were transfected with siRNA-CD300A or pcDNA3.1-CD300A vector to down- or up-regulate the expression of CD300A. Cell Counting Kit 8, colony formation and Transwell assays were used to assess the effects of CD300A on cell proliferation and migration capacities. Flow cytometry was performed to examine rate of apoptosis, and the protein levels of associated proteins was detected using Western blot assay.
Results: From GEPIA analysis, we observed that expression of CD300A mRNA was downregulated in NSCLC and positively correlated with the overall survival of NSCLC patients. Overexpression of CD300A significantly suppressed cell growth and migration capacities of A549 and H1650 cells and induced cell apoptosis via regulating apoptosis-related proteins. Moreover, decreasing level of CD300A promoted cell growth and migration and blocked apoptosis of NSCLC cells. Furthermore, upregulation of CD300A led to significant decrease in expression level of Wnt3 and β-catenin, the pivotal components in Wnt/β-catenin signaling pathway, and an increase in expression of E-cad, a key protein in tumor metastasis, in A549 and H1650 cells; while depletion of CD300A up-regulated the Wnt/β-catenin signaling pathway. In conclusion, the present study highlighted an anti-oncogenic role of CD300A in the progression of NSCLC via inhibiting Wnt/β-catenin pathway, suggesting that CD300A might be a potential target for the treatment of NSCLC.
Conclusion: CD300A plays an anti-oncogenic role in the progression of NSCLC through inhibiting the Wnt/β-catenin pathway, suggesting that CD300A might be a potential target for the treatment of NSCLC.
Keywords: non-small-cell lung cancer, CD300A, prognosis, progression
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