Identification of Mir-182-3p/FLI-1 Axis as a Key Signaling in Immune Response in Cervical Cancer: A Comprehensive Bioinformatic Analysis

Int J Mol Sci. 2023 Mar 23;24(7):6032. doi: 10.3390/ijms24076032.

Abstract

miRNAs modulate gene expression and play critical functions as oncomiRs or tumor suppressors. The miR-182-3p is important in chemoresistance and cancer progression in breast, lung, osteosarcoma, and ovarian cancer. However, the role of miR-182-3p in cervical cancer (CC) has not been elucidated.

Aim: To analyze the role of miR-182-3p in CC through a comprehensive bioinformatic analysis.

Methods: Gene Expression Omnibus (GEO) databases were used for the expression analysis. The mRNA targets of miR-182-3p were identified using miRDB, TargetScanHuman, and miRPathDB. The prediction of island CpG was performed using the MethPrimer program. The transcription factor binding sites in the FLI-1 promoter were identified using ConSite+, Alibaba2, and ALGGEN-PROMO. The protein-protein interaction (PPI) analysis was performed in STRING 11.5.

Results: miR-182-3p was significantly overexpressed in CC patients and has potential as a diagnostic. We identified 330 targets of miR-182-3p including FLI-1, which downregulates its expression in CC. Additionally, the aberrant methylation of the FLI-1 promoter and Ap2a transcription factor could be involved in downregulating FLI1 expression. Finally, we found that FLI-1 is a possible key gene in the immune response in CC.

Conclusions: The miR-182-3p/FLI-1 axis plays a critical role in immune response in CC.

Keywords: AP2α; FLI-1; cervical cancer; methylation; miR-182-3p; response immune.

MeSH terms

  • Cell Line, Tumor
  • Cell Proliferation
  • Computational Biology
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Immunity
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • Transcription Factors / metabolism
  • Uterine Cervical Neoplasms* / pathology

Substances

  • MicroRNAs
  • Mirn182 microRNA, human
  • Transcription Factors
  • FLII protein, human

Grants and funding

This research received no external funding.