التفاصيل البيبلوغرافية
| العنوان: |
ETHE1 dampens colorectal cancer angiogenesis by promoting TC45 Dephosphorylation of STAT3 to inhibit VEGF-A expression |
| المؤلفون: |
Xiaowei She, Jialu Xu, Haokun Zhang, Chengxin Yu, Zejun Rao, Jiakun Zhang, Wenli Zhan, Fuqing Hu, Da Song, Haijie Li, Xuelai Luo, Guihua Wang, Junbo Hu, Senyan Lai |
| المصدر: |
Cell Death and Disease, Vol 15, Iss 8, Pp 1-14 (2024) |
| بيانات النشر: |
Nature Publishing Group, 2024. |
| سنة النشر: |
2024 |
| المجموعة: |
LCC:Cytology |
| مصطلحات موضوعية: |
Cytology, QH573-671 |
| الوصف: |
Abstract Angiogenesis is critical for colorectal cancer (CRC) progression, but its mechanisms remain unclear. Here, we reveal that ethylmalonic encephalopathy protein 1 (ETHE1), an essential enzyme in hydrogen sulfide catabolism, inhibits VEGF-A expression and tumor angiogenesis in vitro and in vivo. Moreover, we find that this biological function of ETHE1 depends on the STAT3/VEGF-A pathway. Further investigation demonstrates that ETHE1 promotes the interaction between T cell protein tyrosine phosphatase (TC45) and STAT3, resulting in decreased STAT3 phosphorylation and inhibition of the STAT3 signaling pathway. In clinical samples, we find that ETHE1 is downregulated in CRC and positively correlates with survival outcomes of CRC patients. Meanwhile, the negative correlation of ETHE1 and VEGF-A expression is verified in CRC specimens, and the patients with low ETHE1 and high VEGF-A expression exhibits poorer prognosis. Collectively, our study identifies ETHE1 as a novel regulator of tumor angiogenesis, implying its potential as a prognostic biomarker and promising antiangiogenic target for CRC patients. |
| نوع الوثيقة: |
article |
| وصف الملف: |
electronic resource |
| اللغة: |
English |
| تدمد: |
2041-4889 |
| Relation: |
https://doaj.org/toc/2041-4889 |
| DOI: |
10.1038/s41419-024-07021-w |
| URL الوصول: |
https://doaj.org/article/5085fbddf85a4f72bcc353e3c1b2dfce |
| رقم الانضمام: |
edsdoj.5085fbddf85a4f72bcc353e3c1b2dfce |
| قاعدة البيانات: |
Directory of Open Access Journals |
Full Text Finder