MUC3A promotes the progression of cholangiocarcinoma through the MAPK/ERK pathway

Abstract Aim Cholangiocarcinoma (CCA) is the most common malignant tumor of the bile ducts. Due to its anatomical location, growth pattern, and lack of clear diagnostic criteria, it presents diagnostic challenges. Exploring its occurrence and development to find early markers and treatment targets i...

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Main Authors: Baijie Feng, Wei Su, Lina Hu, Minghua Yu
Format: Article
Language:English
Published: Springer 2025-04-01
Series:Discover Oncology
Subjects:
Online Access:https://doi.org/10.1007/s12672-025-02199-7
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author Baijie Feng
Wei Su
Lina Hu
Minghua Yu
author_facet Baijie Feng
Wei Su
Lina Hu
Minghua Yu
author_sort Baijie Feng
collection DOAJ
description Abstract Aim Cholangiocarcinoma (CCA) is the most common malignant tumor of the bile ducts. Due to its anatomical location, growth pattern, and lack of clear diagnostic criteria, it presents diagnostic challenges. Exploring its occurrence and development to find early markers and treatment targets is of great significance. Methods To determine whether Mucin 3A (MUC3A) can regulate the occurrence and development of cholangiocarcinoma cells and its mechanism, we compared the expression levels of MUC3A between intrahepatic biliary epithelial cells and cholangiocarcinoma cells and constructed stable transfections of KONC (transfection negative control group) and MUC3A-KO1 and KO2 (transfection MUC3A knockout vectors) lentivirus in CCA cell lines. We investigated the effect of MUC3A on the proliferative capacity of cholangiocarcinoma cells using the CCK-8 assay and colony formation assay. The regulatory effect of MUC3A on the cell cycle of cholangiocarcinoma cells was examined using flow cytometry. The impact of MUC3A on the invasion and migration of cholangiocarcinoma cells was observed through scratch and Transwell assays. Additionally, the mechanism by which MUC3A regulates proliferation and metastasis of cholangiocarcinoma was explored using Western blot. Results MUC3A is highly expressed in cholangiocarcinoma. MUC3A promotes the proliferation of cholangiocarcinoma cells by regulating the cell cycle. Additionally, MUC3A enhances the invasion and migration of cholangiocarcinoma cells by regulating the epithelial-mesenchymal transition. Furthermore, MUC3A regulates the proliferation and metastasis of cholangiocarcinoma cells through the ERK signaling pathway. Conclusions This study demonstrates that MUC3A regulates the proliferation and metastasis of cholangiocarcinoma cells through the ERK signaling pathway.
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spelling doaj-art-8bec56e7ef5b4606a611ea645b5560bc2025-08-20T02:11:42ZengSpringerDiscover Oncology2730-60112025-04-0116111310.1007/s12672-025-02199-7MUC3A promotes the progression of cholangiocarcinoma through the MAPK/ERK pathwayBaijie Feng0Wei Su1Lina Hu2Minghua Yu3Fudan University Clinical Research Center for Cell-Based Immunotherapy & Department of Oncology, Fudan University Pudong Medical CenterDepartment of Medical Oncology, Fudan University Shanghai Cancer CenterFudan University Clinical Research Center for Cell-Based Immunotherapy & Department of Oncology, Fudan University Pudong Medical CenterFudan University Clinical Research Center for Cell-Based Immunotherapy & Department of Oncology, Fudan University Pudong Medical CenterAbstract Aim Cholangiocarcinoma (CCA) is the most common malignant tumor of the bile ducts. Due to its anatomical location, growth pattern, and lack of clear diagnostic criteria, it presents diagnostic challenges. Exploring its occurrence and development to find early markers and treatment targets is of great significance. Methods To determine whether Mucin 3A (MUC3A) can regulate the occurrence and development of cholangiocarcinoma cells and its mechanism, we compared the expression levels of MUC3A between intrahepatic biliary epithelial cells and cholangiocarcinoma cells and constructed stable transfections of KONC (transfection negative control group) and MUC3A-KO1 and KO2 (transfection MUC3A knockout vectors) lentivirus in CCA cell lines. We investigated the effect of MUC3A on the proliferative capacity of cholangiocarcinoma cells using the CCK-8 assay and colony formation assay. The regulatory effect of MUC3A on the cell cycle of cholangiocarcinoma cells was examined using flow cytometry. The impact of MUC3A on the invasion and migration of cholangiocarcinoma cells was observed through scratch and Transwell assays. Additionally, the mechanism by which MUC3A regulates proliferation and metastasis of cholangiocarcinoma was explored using Western blot. Results MUC3A is highly expressed in cholangiocarcinoma. MUC3A promotes the proliferation of cholangiocarcinoma cells by regulating the cell cycle. Additionally, MUC3A enhances the invasion and migration of cholangiocarcinoma cells by regulating the epithelial-mesenchymal transition. Furthermore, MUC3A regulates the proliferation and metastasis of cholangiocarcinoma cells through the ERK signaling pathway. Conclusions This study demonstrates that MUC3A regulates the proliferation and metastasis of cholangiocarcinoma cells through the ERK signaling pathway.https://doi.org/10.1007/s12672-025-02199-7CholangiocarcinomaMUC3AProliferationMigrationInvasionCell cycle
spellingShingle Baijie Feng
Wei Su
Lina Hu
Minghua Yu
MUC3A promotes the progression of cholangiocarcinoma through the MAPK/ERK pathway
Discover Oncology
Cholangiocarcinoma
MUC3A
Proliferation
Migration
Invasion
Cell cycle
title MUC3A promotes the progression of cholangiocarcinoma through the MAPK/ERK pathway
title_full MUC3A promotes the progression of cholangiocarcinoma through the MAPK/ERK pathway
title_fullStr MUC3A promotes the progression of cholangiocarcinoma through the MAPK/ERK pathway
title_full_unstemmed MUC3A promotes the progression of cholangiocarcinoma through the MAPK/ERK pathway
title_short MUC3A promotes the progression of cholangiocarcinoma through the MAPK/ERK pathway
title_sort muc3a promotes the progression of cholangiocarcinoma through the mapk erk pathway
topic Cholangiocarcinoma
MUC3A
Proliferation
Migration
Invasion
Cell cycle
url https://doi.org/10.1007/s12672-025-02199-7
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