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已发表论文
炎症性肠病与乳腺癌的常见生物标志物及发病机制：孟德尔随机化与多组学研究
Authors Zhang D, Guan Y, Tang H, Xue Q, Li X, Bin X, You F
Received 11 June 2025
Accepted for publication 26 November 2025
Published 8 December 2025 Volume 2025:17 Pages 1183—1197
DOI https://doi.org/10.2147/BCTT.S546371
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Harikrishna Nakshatri
Daqing Zhang,1 Yongjun Guan,1 Haitao Tang,2 Qingze Xue,2 Xiaoqiang Li,2 Xu Bin,3 Faping You2
1Department of General Surgery, Beijing Friendship Hospital, Capital Medical University,State Key Lab of Digestive Health,National Clinical Research Center for Digestive Diseases, Beijing, People’s Republic of China; 2Department of Breast Surgery, Shengli Oilfield Central Hospital, Dongying, Shandong, People’s Republic of China; 3Department of Pathology, Shengli Oilfield Central Hospital, Dongying, Shandong, People’s Republic of China
Correspondence: Faping You, Email yfaping@163.com Xu Bin, Email xub_china@126.com
Background: Inflammatory bowel disease (IBD) and breast cancer represent significant global health burdens. Although epidemiological studies have suggested a potential link between them, the causal relationship and underlying molecular mechanisms remain unclear. This study employed Mendelian randomization (MR) and multi-omics approaches to investigate the causal association between IBD and breast cancer and to explore shared genetic biomarkers and pathological pathways.
Methods: A two-sample MR analysis was performed using genome-wide association study (GWAS) data. Shared genes were identified and validated using the GEO and TCGA databases. THBS3 expression was further verified in human breast cancer tissues via immunohistochemistry and RT-PCR. Immune infiltration analysis, drug sensitivity assessment, molecular docking, ceRNA network construction, and pathway enrichment analyses (GSEA and GSVA) were conducted to explore the functional role of THBS3.
Results: MR analysis indicated that IBD significantly increases the risk of breast cancer. THBS3 was identified as a commonly overexpressed gene in both diseases and was associated with poor prognosis. THBS3-high breast cancer patients exhibited resistance to Dinaciclib, Daporinad, and Rapamycin. Molecular docking and dynamics simulations confirmed a strong binding affinity between THBS3 and Rapamycin. A ceRNA network linked THBS3 to miR-423-5p and chemotherapy resistance-related lncRNAs. Pathway analyses revealed THBS3 involvement in extracellular matrix receptor interaction and proteasome pathways.
Conclusion: This study provides genetic evidence supporting IBD as a risk factor for breast cancer and highlights THBS3 as a key shared biomarker. THBS3 may promote breast cancer progression through immune regulation, ECM remodeling, and drug resistance mechanisms, suggesting its potential as a therapeutic target. These findings support enhanced breast cancer screening in IBD patients.
Keywords: IBD, Crohn’s disease, ulcerative colitis, breast cancer, Mendelian randomization
1Department of General Surgery, Beijing Friendship Hospital, Capital Medical University,State Key Lab of Digestive Health,National Clinical Research Center for Digestive Diseases, Beijing, People’s Republic of China; 2Department of Breast Surgery, Shengli Oilfield Central Hospital, Dongying, Shandong, People’s Republic of China; 3Department of Pathology, Shengli Oilfield Central Hospital, Dongying, Shandong, People’s Republic of China
Correspondence: Faping You, Email yfaping@163.com Xu Bin, Email xub_china@126.com
Background: Inflammatory bowel disease (IBD) and breast cancer represent significant global health burdens. Although epidemiological studies have suggested a potential link between them, the causal relationship and underlying molecular mechanisms remain unclear. This study employed Mendelian randomization (MR) and multi-omics approaches to investigate the causal association between IBD and breast cancer and to explore shared genetic biomarkers and pathological pathways.
Methods: A two-sample MR analysis was performed using genome-wide association study (GWAS) data. Shared genes were identified and validated using the GEO and TCGA databases. THBS3 expression was further verified in human breast cancer tissues via immunohistochemistry and RT-PCR. Immune infiltration analysis, drug sensitivity assessment, molecular docking, ceRNA network construction, and pathway enrichment analyses (GSEA and GSVA) were conducted to explore the functional role of THBS3.
Results: MR analysis indicated that IBD significantly increases the risk of breast cancer. THBS3 was identified as a commonly overexpressed gene in both diseases and was associated with poor prognosis. THBS3-high breast cancer patients exhibited resistance to Dinaciclib, Daporinad, and Rapamycin. Molecular docking and dynamics simulations confirmed a strong binding affinity between THBS3 and Rapamycin. A ceRNA network linked THBS3 to miR-423-5p and chemotherapy resistance-related lncRNAs. Pathway analyses revealed THBS3 involvement in extracellular matrix receptor interaction and proteasome pathways.
Conclusion: This study provides genetic evidence supporting IBD as a risk factor for breast cancer and highlights THBS3 as a key shared biomarker. THBS3 may promote breast cancer progression through immune regulation, ECM remodeling, and drug resistance mechanisms, suggesting its potential as a therapeutic target. These findings support enhanced breast cancer screening in IBD patients.
Keywords: IBD, Crohn’s disease, ulcerative colitis, breast cancer, Mendelian randomization