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IGF2BP1 promotes SRF-dependent transcription in cancer in a m6A- and miRNA-dependent manner

Simon Müller1, Markus Glaß1, Anurag K Singh2

  • 1Institute of Molecular Medicine, Section for Molecular Cell Biology, Faculty of Medicine, Martin Luther University Halle-Wittenberg, Charles Tanford protein center, Kurt-Mothes-Str. 3a, 06120 Halle, Germany.

Nucleic Acids Research
|October 30, 2018
PubMed

Insights

The oncofetal protein IGF2BP1 enhances cancer growth by stabilizing SRF mRNA, boosting tumor cell proliferation and invasion. This N6-methyladenosine-dependent mechanism reveals a key oncogenic network in various cancers.

Area of Science:

  • Molecular oncology
  • Gene regulation
  • Cancer biology

Background:

  • IGF2BP1 is an oncofetal protein.
  • SRF is a transcriptional regulator.
  • Both play roles in cancer progression.

Purpose of the Study:

  • To investigate the functional relationship between IGF2BP1 and SRF in cancer.
  • To elucidate the regulatory mechanisms governing SRF expression by IGF2BP1.
  • To identify downstream targets and clinical implications of the SRF/IGF2BP1 axis.

Main Methods:

  • Investigated IGF2BP1's role in SRF mRNA regulation.
  • Utilized N6-methyladenosine (m6A) and miRNA-directed decay assays.
  • Analyzed SRF-target gene expression and their correlation with patient survival.

Main Results:

  • IGF2BP1 stabilizes SRF mRNA in an m6A-dependent manner, preventing miRNA-mediated decay.
  • This leads to increased SRF transcriptional activity, promoting tumor cell growth and invasion.
  • Upregulation of SRF/IGF2BP1-dependent genes (e.g., PDLIM7, FOXK1) correlates with poor survival in ovarian, liver, and lung cancers.

Conclusions:

  • The SRF/IGF2BP1 axis, regulated by m6A and miRNAs, drives cancer progression.
  • This network represents a conserved oncogenic driver in multiple cancer types.
  • Targeting this pathway may offer therapeutic strategies for cancer treatment.

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