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YB-1 activating cascades as potential targets in KRAS-mutated tumors

Shayan Khozooei1, Soundaram Veerappan1, Mahmoud Toulany2

  • 1Division of Radiobiology and Molecular Environmental Research, Department of Radiation Oncology, University of Tuebingen, Tuebingen, Germany.

Strahlentherapie Und Onkologie : Organ Der Deutschen Rontgengesellschaft ... [Et Al]
|June 2, 2023
PubMed

Insights

Y-box binding protein-1 (YB-1) is crucial for cancer cell processes and response to chemoradiotherapy (CRT). Targeting the KRAS/YB-1 pathway may improve CRT outcomes in KRAS-mutated solid tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Y-box binding protein-1 (YB-1) is a multifunctional protein highly expressed in various human solid tumors.
  • YB-1 regulates critical cellular processes including cell cycle progression, cancer stemness, and DNA damage signaling, all vital for chemoradiotherapy (CRT) response.
  • KRAS mutations are prevalent in cancers, and oncogenic KRAS is known to mediate resistance to CRT.

Purpose of the Study:

  • To review the significance of the KRAS/YB-1 signaling cascade in KRAS-mutated solid tumors' response to CRT.
  • To explore potential therapeutic strategies targeting the KRAS/YB-1 pathway to enhance CRT efficacy.

Main Methods:

  • Literature review focusing on the interplay between KRAS, YB-1, and CRT response.
  • Analysis of current research on kinases downstream of KRAS, such as AKT and p90 ribosomal S6 kinase, and their role in YB-1 phosphorylation.

Main Results:

  • A strong correlation exists between KRAS mutation status and YB-1 activity.
  • Oncogenic KRAS signaling activates downstream kinases that phosphorylate YB-1, influencing CRT resistance.
  • The KRAS/YB-1 cascade is a key determinant of treatment response in KRAS-mutated solid tumors.

Conclusions:

  • The KRAS/YB-1 pathway plays a pivotal role in the response of KRAS-mutated solid tumors to chemoradiotherapy.
  • Interfering with the KRAS/YB-1 cascade presents a promising therapeutic avenue for improving CRT outcomes in these patients.
Keywords:
ChemoradiotherapyDNA damage response signalingMolecular targetingOncogenic KRASY‑box binding protein‑1

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