Breast cancer (Dove Medical Press) · 2026
Cytoplasmic Basigin Localization is Associated with EMT, Tumor Budding, and Adverse Prognosis in Breast Cancer.
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Xu Xiaoyan, Zhang Yaozhong, Fang Huijuan, Xu Xianwei, Jiang Huang, Liu Shuguang
Аннотация
PURPOSE: To investigate the clinicopathological significance of Basigin subcellular localization in breast invasive ductal carcinoma, with particular emphasis on its association with epithelial-mesenchymal transition (EMT), tumor budding, and patient prognosis.
METHODS: A total of 206 cases of primary breast invasive ductal carcinoma were retrospectively collected from Zhengzhou People's Hospital between January 2014 and January 2024. Immunohistochemistry was performed to evaluate the expression and subcellular localization of Basigin, E-cadherin, and Vimentin. Tumor budding was assessed according to the International Tumor Budding Consensus Conference (ITBCC) criteria. Associations between marker expression, clinicopathological parameters, and disease-free survival (DFS) were analyzed. A prognostic nomogram was subsequently constructed based on independent prognostic factors identified by multivariate Cox regression analysis.
RESULTS: Predominantly cytoplasmic Basigin localization was significantly associated with larger tumor size, higher Nottingham grade, high-grade tumor budding, advanced TNM stage, and HER2-overexpressing/triple-negative subtypes (all P < 0.05). Tumor budding regions exhibited EMT-associated phenotypes characterized by reduced membranous Basigin staining with relative cytoplasmic redistribution, decreased E-cadherin expression, and increased Vimentin expression. Distinct tumor budding patterns were observed among molecular subtypes, with luminal tumors predominantly showing no budding, HER2-overexpressing tumors showing cluster budding, and triple-negative tumors predominantly showing single-cell budding (all P < 0.05). Kaplan-Meier and multivariate Cox regression analyses demonstrated that Basigin localization (HR = 0.380, 95% CI: 0.171-0.844, P = 0.017), Nottingham grade (HR = 4.839, 95% CI: 2.238-10.466, P < 0.001), tumor budding grade (HR = 37.932, 95% CI: 12.850-111.966, P < 0.001), and molecular subtype (HR = 1.523, 95% CI: 1.164-1.991, P = 0.002) were independent prognostic factors for disease-free survival (DFS). The nomogram demonstrated strong predictive performance, with area under the curve (AUC) values of 0.919, 0.921, and 0.980 for predicting 2-, 3-, and 5-year DFS, respectively.
CONCLUSION: Basigin subcellular redistribution is significantly associated with EMT-associated phenotypes, tumor budding, and adverse prognosis in breast cancer. Assessment of Basigin localization may provide additional prognostic value beyond conventional clinicopathological parameters. A nomogram integrating Basigin localization, tumor budding, histological grade, and molecular subtype may facilitate individualized risk stratification in patients with breast cancer, pending external validation in independent cohorts.
METHODS: A total of 206 cases of primary breast invasive ductal carcinoma were retrospectively collected from Zhengzhou People's Hospital between January 2014 and January 2024. Immunohistochemistry was performed to evaluate the expression and subcellular localization of Basigin, E-cadherin, and Vimentin. Tumor budding was assessed according to the International Tumor Budding Consensus Conference (ITBCC) criteria. Associations between marker expression, clinicopathological parameters, and disease-free survival (DFS) were analyzed. A prognostic nomogram was subsequently constructed based on independent prognostic factors identified by multivariate Cox regression analysis.
RESULTS: Predominantly cytoplasmic Basigin localization was significantly associated with larger tumor size, higher Nottingham grade, high-grade tumor budding, advanced TNM stage, and HER2-overexpressing/triple-negative subtypes (all P < 0.05). Tumor budding regions exhibited EMT-associated phenotypes characterized by reduced membranous Basigin staining with relative cytoplasmic redistribution, decreased E-cadherin expression, and increased Vimentin expression. Distinct tumor budding patterns were observed among molecular subtypes, with luminal tumors predominantly showing no budding, HER2-overexpressing tumors showing cluster budding, and triple-negative tumors predominantly showing single-cell budding (all P < 0.05). Kaplan-Meier and multivariate Cox regression analyses demonstrated that Basigin localization (HR = 0.380, 95% CI: 0.171-0.844, P = 0.017), Nottingham grade (HR = 4.839, 95% CI: 2.238-10.466, P < 0.001), tumor budding grade (HR = 37.932, 95% CI: 12.850-111.966, P < 0.001), and molecular subtype (HR = 1.523, 95% CI: 1.164-1.991, P = 0.002) were independent prognostic factors for disease-free survival (DFS). The nomogram demonstrated strong predictive performance, with area under the curve (AUC) values of 0.919, 0.921, and 0.980 for predicting 2-, 3-, and 5-year DFS, respectively.
CONCLUSION: Basigin subcellular redistribution is significantly associated with EMT-associated phenotypes, tumor budding, and adverse prognosis in breast cancer. Assessment of Basigin localization may provide additional prognostic value beyond conventional clinicopathological parameters. A nomogram integrating Basigin localization, tumor budding, histological grade, and molecular subtype may facilitate individualized risk stratification in patients with breast cancer, pending external validation in independent cohorts.