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.

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