دورية أكاديمية

OTUD7B knockdown inhibits proliferation and autophagy through AKT/mTOR signaling pathway in human prostate cancer cell

التفاصيل البيبلوغرافية
العنوان: OTUD7B knockdown inhibits proliferation and autophagy through AKT/mTOR signaling pathway in human prostate cancer cell
المؤلفون: Yae Ji Kim, Hui Ju Lee, Kyung Hyun Kim, Sung Pil Cho, Ju Young Jung
المصدر: Discover Oncology, Vol 15, Iss 1, Pp 1-8 (2024)
بيانات النشر: Springer, 2024.
سنة النشر: 2024
المجموعة: LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
مصطلحات موضوعية: Autophagy, Prostate cancer, Proliferation, mTOR, OTUD7B, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
الوصف: Abstract Prostate cancer (PCa) is the second leading disease of cancer-related death in men around the world, and it is almost impossible to treat advanced PCa. OTUD7B is a member of the deubiquitinase family that undergoes a post-translational transformation process, which is essential for cell stability and signaling and is known to play a critical role in cancer. However, its role in PCa has not been discovered. The aim of the study was to investigate the expression and mechanism of OTUD7B in PCa cells. According to the database, high OTUD7B expression showed a poor prognosis. Therefore, we downregulated OTUD7B using siRNA and confirmed the role of OTUD7B in PC3 prostate cancer cells. OTUD7B knockdown effectively induced apoptosis and inhibited the proliferation in PC3 cells. OTUD7B knockdown inhibited autophagy through AKT/mTOR signaling. We also confirmed the relationship between AKT/mTOR signaling and autophagy through rapamycin, an mTOR inhibitor. Taken together, OTUD7B promotes the proliferation, and autophagy, and inhibits apoptosis of prostate cancer cells via the AKT/mTOR signaling pathway.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2730-6011
Relation: https://doaj.org/toc/2730-6011
DOI: 10.1007/s12672-024-01073-2
URL الوصول: https://doaj.org/article/136bf4db124e44989c20dd9fa0bfef00
رقم الأكسشن: edsdoj.136bf4db124e44989c20dd9fa0bfef00
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:27306011
DOI:10.1007/s12672-024-01073-2