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Transforming growth factor-β (TGFβ) signaling acts as suppressor and inducer of tumor progression during the early and late stages of cancer, respectively. Some miRNAs have shown a regulatory effect on TGFβ signaling and here, we have used a combination of bioinformatics and experimental tools to show that  hsa-miR-5590-3p  is a regulator of multiple genes expression in the TGFβ signaling pathway. Consistent with the bioinformatics predictions,  hsa-miR-5590-3p  had a negative correlation of expression with  TGFβ-R1 ,  TGFβ-R2 ,  SMAD3  and  SMAD4  genes, detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Then, the dual luciferase assay supported the direct interaction between  hsa-miR-5590-3p  and  TGFβ-R1 ,  TGFβ-R2 ,  SMAD3  and  SMAD4 -3′UTR sequences. Consistently, the TGFβ-R1 protein level was reduced following the overexpression of  hsa-miR-5590-3p , detected by Western analysis. Also,  hsa-miR-5590-3p  overexpression brought about the downregulation of  TGFβ-R1 ,  TGFβ-R2 ,  SMAD3  and  SMAD4  expression in HCT-116 cells, detected by RT-qPCR, followed by cell cycle arrest in the sub-G1 phase, detected by flow cytometry. RT-qPCR results indicated that  hsa-miR-5590-3p  is significantly downregulated in breast tumor tissues (late stage) compared to their normal pairs. Altogether, data introduces  hsa-miR-5590-3p  as a negative regulator of the TGFβ/SMAD signaling pathway which acts through downregulation of  TGFβ-R1 ,  TGFβ-R2 ,  SMAD3  and  SMAD4  transcripts. Therefore, it can be tested as a therapy target in cancers in which the TGFβ/SMAD pathway is deregulated.

Regulatory effect of hsa-miR-5590-3P on TGFβ signaling through targeting of TGFβ-R1, TGFβ-R2, SMAD3 and SMAD4 transcripts