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PI4KIIIβ is a therapeutic target in chromosome 1q-amplified lung adenocarcinoma

Xiaochao Tan1, Priyam Banerjee1, Edward A Pham2

  • 1Department of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.

Science Translational Medicine
|January 24, 2020
PubMed

Insights

Cancer cells amplify chromosome 1q, increasing secretion via phosphatidylinositol (PI)-4-kinase IIIβ (PI4KIIIβ). Inhibiting PI4KIIIβ triggers cancer cell death and halts tumor growth and metastasis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Malignant cells exhibit increased secretion of protumorigenic proteins, but the underlying mechanisms and therapeutic relevance are not fully understood.
  • Chromosome 1q amplifications are common in various cancers and involve genes regulating secretory pathways.

Purpose of the Study:

  • To investigate the role of chromosome 1q-amplified genes in cancer cell secretion and progression.
  • To identify molecular targets for therapeutic intervention in cancers with 1q amplifications.

Main Methods:

  • Molecular, biochemical, and cell biological analyses were performed.
  • Investigated the function of phosphatidylinositol (PI)-4-kinase IIIβ (PI4KIIIβ) in cancer cells.
  • Utilized selective PI4KIIIβ antagonists to assess therapeutic efficacy.

Main Results:

  • Identified a frequently amplified 1q region encoding PI4KIIIβ, a key regulator of secretory vesicle biogenesis.
  • PI4KIIIβ-derived PI-4-phosphate (PI4P) enhances secretion and lung adenocarcinoma progression via Golgi phosphoprotein 3 (GOLPH3).
  • PI4KIIIβ inhibition induced apoptosis, suppressed tumor growth, and reduced metastasis in 1q-amplified cancer cells.

Conclusions:

  • Chromosome 1q amplifications create a dependency on PI4KIIIβ-mediated secretion for cancer cell survival and progression.
  • Targeting PI4KIIIβ represents a potential therapeutic strategy for cancers with 1q amplifications.

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