MiR-15a and miR-16 induce autophagy and enhance chemosensitivity of Camptothecin
| Autor: | Wei Qiu, Naihan Xu, Weidong Xie, Jiangbin Wu, Nunu Huang, Qing Lyu, Jie He, Yaou Zhang |
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| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
Cancer Research
Programmed cell death autophagy Rictor HeLa Cell Line Tumor medicine Humans 3' Untranslated Regions PI3K/AKT/mTOR pathway Pharmacology Binding Sites biology microRNA Base Sequence Chemistry Cell growth Autophagy biology.organism_classification Antineoplastic Agents Phytogenic Cell biology MicroRNAs cell proliferation Rapamycin-Insensitive Companion of mTOR Protein Oncology Apoptosis Drug Resistance Neoplasm Gene Knockdown Techniques Cancer cell Cancer research mTOR Molecular Medicine Camptothecin RNA Interference Carrier Proteins medicine.drug Research Paper HeLa Cells |
| Zdroj: | Cancer Biology & Therapy |
| ISSN: | 1555-8576 1538-4047 |
| Popis: | It has been reported that persistent or excessive autophagy promotes cancer cell death during chemotherapy, either by enhancing the induction of apoptosis or mediating autophagic cell death. Here, we show that miR-15a and miR-16 are potent inducers of autophagy. Rictor, a component of mTORC2 complex, is directly targeted by miR-15a/16. Overexpression of miR-15a/16 or depletion of endogenous Rictor attenuates the phosphorylation of mTORC1 and p70S6K, inhibits cell proliferation and G1/S cell cycle transition in human cervical carcinoma HeLa cells. Moreover, miR-15a/16 dramatically enhances anticancer drug camptothecin (CPT)-induced autophagy and apoptotic cell death in HeLa cells. Collectively, these data demonstrate that miR-15a/16 induced autophagy contribute partly to their inhibition of cell proliferation and enhanced chemotherapeutic efficacy of CPT. |
| Databáze: | OpenAIRE |
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