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API5 confers cancer stem cell-like properties through the FGF2-NANOG axis.

K-H Song1,2,3, H Cho4,5,6, S Kim7

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Oncogenesis
|January 17, 2017
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Apoptosis inhibitor-5 (API5) links tumor immune resistance and cancer stem cell (CSC)-like traits. Blocking FGFR signaling effectively targets API5-high cancers, offering a new therapeutic strategy for refractory tumors.

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Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Tumor evolution under immune selection promotes immune resistance and cancer stem cell (CSC)-like phenotypes.
  • Apoptosis inhibitor-5 (API5) is an immune escape factor, but its role in CSC properties is unclear.

Purpose of the Study:

  • To investigate the functional association between API5 and CSC-like properties.
  • To elucidate the molecular mechanisms linking API5, immune resistance, and CSC traits.
  • To evaluate FGFR signaling blockade as a therapeutic strategy for API5-high cancers.

Main Methods:

  • Assessed API5's role in conferring CSC-like properties (NANOG expression, CD44+ cells, sphere formation).
  • Investigated the dependency on FGFR1 signaling, E2F1, and FGF2 expression.
  • Identified the FGF2-NANOG molecular axis downstream of API5 signaling.
  • Evaluated FGFR signaling blockade in API5-high human cancers.

Main Results:

  • API5 confers CSC-like properties, including NANOG expression, CD44+ cell frequency, and sphere formation.
  • API5-mediated CSC properties depend on FGFR1 signaling activated by E2F1-driven FGF2.
  • The FGF2-NANOG axis is a downstream effector of API5 signaling, conserved in cervical cancer.
  • FGFR signaling blockade effectively controls API5-high human cancers.

Conclusions:

  • API5 plays a critical role in connecting tumor immune resistance with CSC-like properties.
  • The API5-FGFR1-FGF2-NANOG pathway is a key mechanism driving aggressive cancer phenotypes.
  • Targeting FGFR signaling presents a promising therapeutic approach for API5-positive refractory tumors.