[The Effect of MiR-100-5p on the Biological Behaviors of Pediatric Acute Myeloid Leukemia Cells by Targeting IGF1R].

OBJECTIVE

To investigate the effect of miR-100-5p on the biological behaviors of pediatric acute myeloid leukemia (AML) cells by targeting insulin-like growth factor 1 receptor (IGF1R ).

METHODS

QRT-PCR was used to detect the expression levels of miR-100-5p and IGF1R mRNA in AML cell lines (THP-1, TF-1a, HL-60) and serum of children with AML. The dual-luciferase reporter gene assay was applied to verify the targeting relationship between miR-100-5p and IGF1R . THP-1 cells were assigned into Control group, miR-NC group, miR-100-5p mimics group, miR-100-5p mimics+pcDNA group, and miR-100-5p mimics+IGF1R group. The colony formation assay, scratch healing assay, and transwell assay were used to detect the proliferation, migration, and invasion abilities of THP-1 cells in each group, and Western blot assay was used to detect the protein expression of IGF1R, PCNA, MMP-2, MMP-9, E-cadherin, N-cadherin, and Vimentin.

RESULTS

The expression level of IGF1R mRNA was significantly increased, while the expression level of miR-100-5p was significantly decreased in both the serum of pediatric AML patients and THP-1 cells (P < 0.001). Analysis via the StarBase database predicted the presence of potential binding sites between miR-100-5p and IGF1R . Compared with the miR-NC group, in the miR-100-5p mimics group, the number of colonies formed, scratch healing rate, and number of invasive cells of THP-1 cells were significantly decreased; the protein expression levels of IGF1R, PCNA, MMP-2, MMP-9, N-cadherin, and Vimentin were significantly decreased, while the expression level of miR-100-5p and the protein expression level of E-cadherin were significantly increased (all P < 0.05). Compared with the miR-100-5p mimics+pcDNA group, in the miR-100-5p mimics+IGF1R group, the number of colonies formed, scratch healing rate, and number of invasive cells were significantly increased; the protein expression levels of IGF1R, PCNA, MMP-2, MMP-9, N-cadherin, and Vimentin were significantly increased, while the protein expression level of E-cadherin was significantly decreased (all P < 0.05).

CONCLUSION

Overexpression of miR-100-5p can targetedly inhibit IGF1R , thereby suppressing the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of AML cells.