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ILF3 is a substrate of SPOP for regulating serine biosynthesis in colorectal cancer

Kai Li1,2, Jian-Lin Wu3, Baifu Qin1,2

  • 1Guangdong Provincial Key laboratory of Colorectal and Pelvic Floor Disease, The Sixth Affiliated Hospital of Sun Yat-sen University, 510655, Guangzhou, China.

Cell Research
|November 28, 2019
PubMed

Insights

Interleukin enhancer-binding factor 3 (ILF3) drives colorectal cancer (CRC) by stabilizing Serine-Glycine-One-Carbon (SGOC) pathway genes. Inhibiting ILF3 or targeting the EGF-ERK pathway shows promise for CRC treatment.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • The Serine-Glycine-One-Carbon (SGOC) pathway is crucial for anabolism but is often deregulated in cancer.
  • The precise mechanisms by which oncogenes disrupt SGOC metabolism in colorectal cancer (CRC) are not fully understood.

Purpose of the Study:

  • To investigate the role of Interleukin enhancer-binding factor 3 (ILF3) in CRC pathogenesis.
  • To elucidate the mechanism by which ILF3 regulates the SGOC pathway and its implications for tumor growth.

Main Methods:

  • Analysis of ILF3 expression in CRC patient specimens.
  • Investigating ILF3's effect on SGOC gene mRNA stability.
  • Studying the regulation of ILF3 stability via the EGF-MEK-ERK pathway and SPOP-mediated ubiquitination.
  • Evaluating therapeutic strategies in patient-derived xenografts.

Main Results:

  • ILF3 is overexpressed in CRC and linked to poor prognosis.
  • ILF3 directly enhances SGOC gene expression by stabilizing their mRNA.
  • The EGF-MEK-ERK pathway phosphorylates ILF3, preventing its degradation.
  • Combined inhibition of SGOC and EGFR pathways suppressed tumor growth in xenografts with high ERK-ILF3 levels.

Conclusions:

  • ILF3 deregulation, mediated by EGF-ERK signaling, drives serine metabolic reprogramming in CRC.
  • ILF3 is a potential therapeutic target for CRC, particularly in patients with ILF3 overexpression.

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