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HnRNP C binding to inverted Alu elements protects the transcriptome from pre-mRNA circularization.

Alberto Marini1,2, Consuelo Pitolli1,2, Sabrina Ciccone1

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Heterogeneous nuclear ribonucleoprotein C (hnRNP C) represses circular RNAs (circRNAs) in medulloblastoma. Loss of hnRNP C triggers an antiviral response, suggesting therapeutic potential for targeting hnRNP C in cancer.

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Area of Science:

  • Molecular biology
  • Cancer research
  • RNA biology

Background:

  • Back-splicing drives circular RNA (circRNA) biogenesis, but its regulation in tumors is not fully understood.
  • Circular RNAs play roles in various biological processes, and their dysregulation is implicated in cancer.
  • Group 3 medulloblastoma (MB) is an aggressive pediatric brain tumor with complex molecular underpinnings.

Purpose of the Study:

  • To investigate the role of heterogeneous nuclear ribonucleoprotein C (hnRNP C) in regulating circRNA biogenesis in group 3 MB.
  • To elucidate the molecular mechanisms by which hnRNP C controls circRNA formation.
  • To explore the potential therapeutic implications of targeting hnRNP C in medulloblastoma.

Main Methods:

  • Analysis of hnRNP C binding to Alu elements in pre-mRNA.
  • Assessment of the impact of hnRNP C expression on circRNA and linear RNA levels.
  • Investigation of cytoplasmic double-stranded RNA formation and interferon response.
  • In silico and experimental validation of findings in group 3 MB models.

Main Results:

  • hnRNP C binds Alu elements to repress circRNA biogenesis in group 3 MB.
  • hnRNP C expression levels modulate the balance between linear and circRNA splicing.
  • Loss of hnRNP C leads to cytoplasmic double-stranded RNA accumulation and an antiviral response.
  • Targeting hnRNP C may enhance cancer surveillance through immune activation.

Conclusions:

  • hnRNP C acts as a repressor of circRNA biogenesis, maintaining transcriptome integrity in group 3 MB.
  • Dysregulation of hnRNP C contributes to the oncogenic phenotype by altering RNA splicing patterns.
  • Targeting hnRNP C presents a potential therapeutic strategy for group 3 MB, possibly by inducing an anti-tumor immune response.