Role of Camp in progression of mouse lung cancer and molecular mecha-nism of EMT mediated by TGF-β/Smad pathway
10.3969/j.issn.1000-4718.2025.05.004
- VernacularTitle:Camp在小鼠肺癌进展中的作用及TGF-β/Smad通路介导EMT的分子机制研究
- Author:
Junlu WU
1
;
Yaran LI
;
Linyun WANG
;
Feng LI
Author Information
1. 宁夏医科大学第一临床医学院,宁夏 银川 750004;宁夏医科大学总医院医学实验中心,宁夏 银川 750004;同济大学附属同济医院检验科,上海 200065
- Publication Type:Journal Article
- Keywords:
cathelicidin-related antimicrobial peptide;
epithelial-mesenchymal transition;
lung cancer;
an-giogenesis
- From:
Chinese Journal of Pathophysiology
2025;41(5):861-870
- CountryChina
- Language:Chinese
-
Abstract:
AIM:This study aims to investigate the role of cathelicidin-related antimicrobial peptide(Camp)gene in lung tumors in mice and to elucidate its molecular mechanisms in regulating epithelial-mesenchymal transition(EMT)and the TGF-β/Smad signaling pathway.METHODS:We conducted histological examinations and survival anal-yses using a KrasG12D spontaneous lung cancer mouse model with Camp gene knockout.This model was utilized to assess the impact of Camp on tumor nodule count,volume,and survival rate in mice.At the cellular level,we constructed A549-Camp and H1975-Camp cell lines to evaluate the effects of Camp on the proliferation,migration,and invasion of lung ade-nocarcinoma cells through soft agar colony formation assays,Scratch assays for cell migration rates,and Transwell assays.Additionally,we performed angiogenesis experiments to assess vascular development.At the molecular level,qRT-PCR was employed to detect the expression of angiogenic factors VEGF,bFGF,and TGF-β.Western blot analysis was utilized to examine the effects of Camp on the expression of EMT-related proteins(E-cadherin,N-cadherin,and Snail)and pro-teins associated with the TGF-β/Smad signaling pathway(TGF-β,p-TGF-β,Smad3,and Smad7).RESULTS:Camp gene knockout significantly suppressed lung tumorigenesis in mice,resulting in a decrease in tumor nodule count and vol-ume,as well as an enhancement in survival rates.In vitro,overexpression of Camp stimulated the proliferation,migra-tion,and invasion of lung adenocarcinoma cells.CONCLUSION:Molecular mechanism studies indicated that Camp modulated the expression of EMT-related proteins by influencing the TGF-β/Smad signaling pathway.
