دورية أكاديمية

MicroRNA-185 induces potent autophagy via AKT signaling in hepatocellular carcinoma

التفاصيل البيبلوغرافية
العنوان: MicroRNA-185 induces potent autophagy via AKT signaling in hepatocellular carcinoma
المؤلفون: Li Zhou, Shunai Liu, Ming Han, Shenghu Feng, Jinqiu Liang, Zhongshu Li, Yaru Li, Hongping Lu, Ting Liu, Yanhua Ma, Jun Cheng
المصدر: Tumor Biology, Vol 39 (2017)
بيانات النشر: IOS Press, 2017.
سنة النشر: 2017
المجموعة: LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
مصطلحات موضوعية: Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
الوصف: Studies have demonstrated that microRNA 185 may be a promising therapeutic target in liver cancer. However, its role in hepatocellular carcinoma is largely unknown. In this study, the proliferation of human HepG2 cells was inhibited by transfection of microRNA 185 mimics. Cell-cycle analysis revealed arrest at the G0/G1 phase. Transfection of HepG2 cells with microRNA 185 mimics significantly induced apoptosis. These data confirmed microRNA 185 as a potent cancer suppressor. We demonstrated that microRNA 185 was a compelling inducer of autophagy, for the first time. When cell autophagy was inhibited by chloroquine or 3-methyladenine, microRNA 185 induced more cell apoptosis. MicroRNA 185 acted as a cancer suppressor by regulating AKT1 expression and phosphorylation. Dual-luciferase reporter assays indicated that microRNA 185 suppressed the expression of target genes including RHEB , RICTOR , and AKT1 by directly interacting with their 3′-untranslated regions. Binding site mutations eliminated microRNA 185 responsiveness. Our findings demonstrate a new role of microRNA 185 as a key regulator of hepatocellular carcinoma via autophagy by dysregulation of AKT1 pathway.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1423-0380
10104283
Relation: https://doaj.org/toc/1423-0380
DOI: 10.1177/1010428317694313
URL الوصول: https://doaj.org/article/115813c2149545e894f873e6d5479a3d
رقم الأكسشن: edsdoj.115813c2149545e894f873e6d5479a3d
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14230380
10104283
DOI:10.1177/1010428317694313