Issue |
BIO Web Conf.
Volume 174, 2025
2025 7th International Conference on Biotechnology and Biomedicine (ICBB 2025)
|
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Article Number | 02023 | |
Number of page(s) | 9 | |
Section | Innovations in Therapeutics and Disease Mechanisms | |
DOI | https://doi.org/10.1051/bioconf/202517402023 | |
Published online | 12 May 2025 |
Prognostic Potential of AKR1B1 in triple-negative breast cancer
1 Medical College, Wuhan University of Science and Technology, Wuhan 430065, Hubei, China
2 College of Life Sciences and Health, Wuhan University of Science and Technology, Wuhan 430081, Hubei, P.R. China
* Corresponding author: a xiongjing@wust.edu.cn and b xinghualiao@wust.edu.cn
c liuyimeng@wust.edu.cn d wangjincheng8848@163.com e 19373313073@wust.edu.cn f jiangshu@wust.edu.cn gguohongshan@wust.edu.cn
This research conducts a thorough bioinformatics examination to explore the possible function of Aldose Reductase (AKR1B1) in Triple - Negative Breast Cancer (TNBC). AKR1B1 displays heterogeneous expression patterns across various cancer types, with notably elevated levels in multiple malignancies such as bladder urothelial carcinoma, cholangiocarcinoma, and esophageal carcinoma, yet exhibiting lower expression in breast invasive carcinoma (BRCA). Utilizing the UALCAN and Human Protein Atlas (HPA) databases, a detailed analysis of AKR1B1 in BRCA reveals its distinct expression profile. Significantly, our results imply that AKR1B1 could act as a prospective biomarker in triple - negative breast cancer (TNBC). This is due to its connection with survival results and its co - expression network within this specific cancer subtype. Additionally, we delve into the complex interplay between AKR1B1 and the tumor immune microenvironment. We emphasize its notable link with CD8+ T cells and macrophages. Protein network analysis identifies key proteins interacting with AKR1B1, and experimental validation demonstrates the efficacy of curcumin in inhibiting the proliferation of TNBC cells, thereby suggesting its potential as a therapeutic agent targeting AKR1B1. This study establishes a foundational understanding of AKR1B1’s role in TNBC and paves the way for future experimental validation and therapeutic explorations.
© The Authors, published by EDP Sciences, 2025
This is an Open Access article distributed under the terms of the Creative Commons Attribution License 4.0, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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