The incidence of breast cancer continues to rise each year despite significant advances in diagnosis and treatment. Obesity-associated dysregulated lipid metabolism is believed to contribute to the increasing risk of breast cancer. However, the mechanisms linking lipid dysregulation to breast cancer risk and progression remain to be determined. The family of fatty acid binding proteins (FABPs) evolves to facilitate lipid transport and metabolism. As the predominant isoforms of FABP members expressed in breast tissue, adipose FABP (A-FABP, also known as FABP4) and epithelial FABP (E-FABP, FABP5) have been shown to play critical roles in breast carcinogenesis. In this study, we collected surgical breast tissue samples from 96 women with different subtypes of breast cancer and comprehensively analyzed the expression pattens of FABP4 and FABP5. We found that distinct expression profiles of FABP4 and FABP5 were associated with their unique roles in breast cancer development. FABP4, mainly expressed in breast stroma, especially in adipose tissue, likely supported neighboring tumor cell lymphovascular invasion through secretion from adipocytes. In contrast, FABP5, primarily expressed in epithelial-derived tumor cells, could promote tumor metastasis by enhancing lipid metabolism. Thus, elevated levels of FABP4 and FABP5 may serve as poor prognostic markers for breast cancer. Inhibiting the activity of FABP4 and/or FABP5 may offer a novel strategy for breast cancer therapy.
Expression profiles of FABP4 and FABP5 in breast cancer: clinical implications and perspectives.
FABP4 和 FABP5 在乳腺癌中的表达谱:临床意义和展望
阅读:4
作者:Jiang Xingshan, Xiong Yiqin, Yu Jianyu, Avellino Anthony, Liu Shanshan, Han Xiaochun, Wang Zhaohua, Shilyansky Jonathan S, Curry Melissa A, Hao Jiaqing, Sauter Edward R, Huang Yi, Sugg Sonia L, Li Bing
| 期刊: | Discover Oncology | 影响因子: | 2.900 |
| 时间: | 2025 | 起止号: | 2025 Mar 19; 16(1):357 |
| doi: | 10.1007/s12672-025-02117-x | 研究方向: | 肿瘤 |
| 疾病类型: | 乳腺癌 | ||
特别声明
1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。
2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。
3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。
4、投稿及合作请联系:info@biocloudy.com。
