Background: Triple-negative breast (TNBC) cancer responds poorly to surgery, radiotherapy, chemotherapy, and endocrine therapy, it is considered the subtype of breast cancer with the worst prognosis. This study investigated MAN2A1's role in regulating the proliferation, invasion, and migration of TNBC cells and its clinical significance. Methods: We enrolled 220 TNBC patients treated at our institution from January 2020 to December 2022. MAN2A1 protein expression was detected, and its correlation with TNBC clinicopathological features was analyzed. Western blot and immunohistochemistry measured MAN2A1 protein levels. CCK-8, colony formation, and EdU assays evaluated MAN2A1's impact on TNBC cell proliferation. Wound healing and Transwell assays assessed its effects on migration and invasion. Results: MAN2A1 protein expression positively correlated with TNBC malignancy. MAN2A1 is overexpressed in larger tumors (≥2 cm), lymph node metastasis-positive cases, and advanced-stage (III-IV) patients. Functional assays demonstrated that MAN2A1 overexpression promoted TNBC cell growth, clonogenicity, migration, and invasion, while its knockdown suppressed these processes. Conclusion: This study systematically elucidates the role of MAN2A1 as a key glycosylation-modifying enzyme in promoting the malignant progression of TNBC. The experimental results demonstrate that MAN2A1 drives TNBC development by enhancing cellular proliferation, invasive capacity, and migratory potential, providing a theoretical basis for developing targeted therapeutic strategies against MAN2A1.
| Published in | European Journal of Clinical and Biomedical Sciences (Volume 11, Issue 2) |
| DOI | 10.11648/j.ejcbs.20251102.12 |
| Page(s) | 24-31 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2025. Published by Science Publishing Group |
Triple-negative Breast Cancer, MAN2A1, Proliferation, Invasion, Metastasis
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APA Style
Sun, Y., Rong, T., Wang, B. (2025). The Expression and Role of MAN2A1 in Triple-negative Breast Cancer. European Journal of Clinical and Biomedical Sciences, 11(2), 24-31. https://doi.org/10.11648/j.ejcbs.20251102.12
ACS Style
Sun, Y.; Rong, T.; Wang, B. The Expression and Role of MAN2A1 in Triple-negative Breast Cancer. Eur. J. Clin. Biomed. Sci. 2025, 11(2), 24-31. doi: 10.11648/j.ejcbs.20251102.12
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Download@article{10.11648/j.ejcbs.20251102.12,
author = {Yu Sun and Tianshu Rong and Baoqing Wang},
title = {The Expression and Role of MAN2A1 in Triple-negative Breast Cancer
},
journal = {European Journal of Clinical and Biomedical Sciences},
volume = {11},
number = {2},
pages = {24-31},
doi = {10.11648/j.ejcbs.20251102.12},
url = {https://doi.org/10.11648/j.ejcbs.20251102.12},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ejcbs.20251102.12},
abstract = {Background: Triple-negative breast (TNBC) cancer responds poorly to surgery, radiotherapy, chemotherapy, and endocrine therapy, it is considered the subtype of breast cancer with the worst prognosis. This study investigated MAN2A1's role in regulating the proliferation, invasion, and migration of TNBC cells and its clinical significance. Methods: We enrolled 220 TNBC patients treated at our institution from January 2020 to December 2022. MAN2A1 protein expression was detected, and its correlation with TNBC clinicopathological features was analyzed. Western blot and immunohistochemistry measured MAN2A1 protein levels. CCK-8, colony formation, and EdU assays evaluated MAN2A1's impact on TNBC cell proliferation. Wound healing and Transwell assays assessed its effects on migration and invasion. Results: MAN2A1 protein expression positively correlated with TNBC malignancy. MAN2A1 is overexpressed in larger tumors (≥2 cm), lymph node metastasis-positive cases, and advanced-stage (III-IV) patients. Functional assays demonstrated that MAN2A1 overexpression promoted TNBC cell growth, clonogenicity, migration, and invasion, while its knockdown suppressed these processes. Conclusion: This study systematically elucidates the role of MAN2A1 as a key glycosylation-modifying enzyme in promoting the malignant progression of TNBC. The experimental results demonstrate that MAN2A1 drives TNBC development by enhancing cellular proliferation, invasive capacity, and migratory potential, providing a theoretical basis for developing targeted therapeutic strategies against MAN2A1.
},
year = {2025}
}
TY - JOUR T1 - The Expression and Role of MAN2A1 in Triple-negative Breast Cancer AU - Yu Sun AU - Tianshu Rong AU - Baoqing Wang Y1 - 2025/06/18 PY - 2025 N1 - https://doi.org/10.11648/j.ejcbs.20251102.12 DO - 10.11648/j.ejcbs.20251102.12 T2 - European Journal of Clinical and Biomedical Sciences JF - European Journal of Clinical and Biomedical Sciences JO - European Journal of Clinical and Biomedical Sciences SP - 24 EP - 31 PB - Science Publishing Group SN - 2575-5005 UR - https://doi.org/10.11648/j.ejcbs.20251102.12 AB - Background: Triple-negative breast (TNBC) cancer responds poorly to surgery, radiotherapy, chemotherapy, and endocrine therapy, it is considered the subtype of breast cancer with the worst prognosis. This study investigated MAN2A1's role in regulating the proliferation, invasion, and migration of TNBC cells and its clinical significance. Methods: We enrolled 220 TNBC patients treated at our institution from January 2020 to December 2022. MAN2A1 protein expression was detected, and its correlation with TNBC clinicopathological features was analyzed. Western blot and immunohistochemistry measured MAN2A1 protein levels. CCK-8, colony formation, and EdU assays evaluated MAN2A1's impact on TNBC cell proliferation. Wound healing and Transwell assays assessed its effects on migration and invasion. Results: MAN2A1 protein expression positively correlated with TNBC malignancy. MAN2A1 is overexpressed in larger tumors (≥2 cm), lymph node metastasis-positive cases, and advanced-stage (III-IV) patients. Functional assays demonstrated that MAN2A1 overexpression promoted TNBC cell growth, clonogenicity, migration, and invasion, while its knockdown suppressed these processes. Conclusion: This study systematically elucidates the role of MAN2A1 as a key glycosylation-modifying enzyme in promoting the malignant progression of TNBC. The experimental results demonstrate that MAN2A1 drives TNBC development by enhancing cellular proliferation, invasive capacity, and migratory potential, providing a theoretical basis for developing targeted therapeutic strategies against MAN2A1. VL - 11 IS - 2 ER -
The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, China
The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, China
The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, China
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