Furin-like enzyme dependency in KRAS-mutant colorectal cancer as a target for personalized treatment strategies

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Published on: September 30, 2016

Geraldine Siegfried1, Yiyang Liu2, Zongcheng He3

  • 1University of Bordeaux, Bordeaux Institute of Oncology (BRIC)-UMR1312, Bordeaux, France.

Biochimica Et Biophysica Acta. Reviews on Cancer
|May 29, 2026
PubMed

Insights

Furin-like enzymes regulate KRAS signaling in colorectal cancer. Inhibiting Furin selectively harms KRAS-mutant cancer cells, offering a potential therapeutic strategy for this disease.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signaling

Background:

  • KRAS signaling pathways are critical for oncogenic activity in various cancers.
  • Furin-like enzymes (proprotein convertases) are proteases involved in activating signaling molecules.
  • Furin processes growth factors, cytokines, and receptor tyrosine kinases (RTKs), influencing KRAS signaling.

Purpose of the Study:

  • To review the crosstalk between KRAS signaling and Furin-like enzymes in cancer progression.
  • To highlight the role of Furin in KRAS-mutant colorectal cancer.
  • To explore therapeutic strategies targeting Furin for KRAS-mutant colorectal cancer.

Main Methods:

  • Literature review summarizing current evidence on KRAS-Furin interactions.
  • Analysis of Furin's role in processing growth factors, cytokines, and RTKs.
  • Examination of Furin inhibition effects on KRAS-mutant cancer cell proliferation and survival.

Main Results:

  • Furin inhibition selectively impairs KRAS-mutant colorectal cancer cell proliferation and survival.
  • Furin inhibition disrupts RTK maturation, attenuates downstream signaling, and promotes an immune-stimulatory tumor microenvironment.
  • Furin inhibition blocks maturation of escape pathways, including compensatory RTK activation, repressing KRAS-mutant-mediated resistance.

Conclusions:

  • Furin-like enzymes are key regulators of KRAS signaling and tumor progression.
  • Targeting Furin represents a promising therapeutic approach for KRAS-mutant colorectal cancer.
  • Furin inhibition offers potential for personalized treatment strategies by disrupting oncogenic signaling and immune escape mechanisms.

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