دورية أكاديمية
MicroRNA-185 induces potent autophagy via AKT signaling in hepatocellular carcinoma
العنوان: | MicroRNA-185 induces potent autophagy via AKT signaling in hepatocellular carcinoma |
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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 |
تدمد: | 14230380 10104283 |
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DOI: | 10.1177/1010428317694313 |