miR‑221 inhibits autophagy and targets TP53INP1 in colorectal cancer cells
| Autor: | Xingxiang Pu, Guo Liang Huang, Dan Liao, Congcong Ding, Zhiwei He, Caiguo Ye, Liuyan Zeng, Tong Li, Huahui Li |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Cancer Research Oncogene Cell growth Autophagy Cancer Articles General Medicine Biology Cell cycle medicine.disease_cause medicine.disease 03 medical and health sciences 030104 developmental biology Immunology and Microbiology (miscellaneous) microRNA Cancer research medicine Nuclear protein Carcinogenesis |
| Zdroj: | Experimental and Therapeutic Medicine. |
| ISSN: | 1792-1015 1792-0981 |
| DOI: | 10.3892/etm.2017.5522 |
| Popis: | Colorectal cancer (CRC) is the third most common cancer and the fourth leading cause of cancer-associated mortalities worldwide. MicroRNAs (miRNAs/miRs) serve important roles in tumor development, progression and metastasis. miR-221 has been reported to modulate proliferation, apoptosis, cell cycle distribution and cell migration in a variety of cancers. However, the function of miR-221 in the autophagy of cancer is unclear. In the present study, the role of miR-221 in the autophagy of CRC cells was investigated and its associated target was identified. Survival analysis using The Cancer Genome Atlas data suggested that a higher expression of miR-221 was associated with poor survival in patients with CRC. A Cell Counting kit-8 assay revealed that miR-221 promoted CRC cell proliferation. Autophagy flux analyzed by microtubule-associated protein 1 light chain 3 (LC3) turnover indicated that miR-221 reduced autophagy in CRC cells using different protease inhibitors (E64d and pepstatin A; Bafilomycin A1) in nutrient-rich medium or under starvation conditions. Tumor protein 53-induced nuclear protein 1 (TP53INP1) was identified as a potential novel target of miR-221 by bioinformative prediction. The protein expression of TP53INP1 was inversely regulated by miR-221 in CRC cells. Furthermore, luciferase activity assays were performed and indicated that miR-221 may regulate the luciferase activity of wild-type TP53INP1 without interfering with the activity of mutant TP53INP1. These data suggested that miR-221 may promote the cell proliferation of CRC via the inhibition of autophagy and targeted TP53INP1. |
| Databáze: | OpenAIRE |
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