SEL1L confers reduced EMT and drug resistance to breast cancer cells by promoting Shh degradation
Year: 2025
Type: article
Abstract: settings. Mechanistically, SEL1L suppressed the expression of oncogenic Shh protein by promoting its ubiquitination-proteasomal degradation, thereby inhibiting EMT and improving cellular sensitivity to carboplatin in BRC cells via hedgehog signaling pathway. Our findings emphasize the tumor-suppressive function of endogenous SEL1L in BRC and demonstrate the crucial role of the SEL1L-Shh-Gli1 axis in controlling cancer cell progression, offering a promising foundation for the development of innovative therapeutics against BRC.
Source: iScience
Authors: Hao Zhou, Jie Wang, Xu Wang, Zhaoji Guo, Yan Chen, Erli Gao, Jie Sun, Siying Zhou, Xinyi Guan, Yuxin Wu, Zhe Zhao, Yuting Kuang
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $3,240
Awards: G3004327597, G3029099857
OpenAlex ID: W4415612958