The effect of autophagy-related MicroRNAs on FIP200, ATG13 and HIF1A expression levels in breast cancer patients

Samaneh Ahmadi, Hossein Teimori, Mohammad Hossein Modarressi, Yazdan Asgari, Mojtaba Saffari

Résultats de recherche: Contribution à un journalArticleRevue par des pairs

Résumé

Autophagy acts like a double-edged sword in either tumor promotion or suppression of breast cancer. Crosstalk between miRNAs and autophagic targets is one interesting scenario for the dual behavior of this pathway. On this basis the present study was designed to evaluate the expression pattern of certain candidate miRNAs and their targets in breast cancer patients. A total of 47 fresh breast carcinomas and matched adjacent non-neoplastic tissues were obtained. Bioinformatics analysis of putative miRNA binding sites identified miR-133, and miR-206, miR-199a/b, as regulating expressions of the FIP200, ATG-13 and HIF1a, respectively. The expression levels of candidate miRNAs and their targets were examined using quantitative Real-Time Polymerase Chain Reaction. Our results demonstrated that all four miRNAs expression levels are downregulated in breast tumor tissue compared with corresponding non-neoplastic tissue. Decreased expression of miR-133 and miR-199b showed a significant correlation with tumor grade. Moreover, a significant downregulation of miR-199b was observed in HER-2-negative patients. We found that FIP200 and ATG13 were downregulated in tumor tissues while HIF1a showed a significant upregulation. No significant association between the target genes and clinicopathological features was observed. Our data clarified a strong positive correlation between expression levels of miR-133 and FIP200 while the correlation between miR-206 and ATG13, and, miR-199a/b and HIF1a were not statistically significant. In conclusion, these results support the regulatory role of miR-133 during breast cancer development via the autophagy pathway and provide an opportunity to develop targeted therapeutics for breast cancer.

langue originaleAnglais
Numéro d'article201145
journalHuman Gene
Volume35
Les DOIs
étatPublié - 1 févr. 2023
Modification externeOui

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