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Conditional Reprogramming of Pediatric Human Esophageal Epithelial Cells for Use in Tissue Engineering and Disease Investigation
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Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage

Jung Wook Park1, John K Lee2, Katherine M Sheu3

  • 1Department of Microbiology, Immunology, and Molecular Genetics, University of California-Los Angeles, Los Angeles, CA 90095, USA.

Science (New York, N.Y.)
|October 6, 2018
PubMed

Insights

Potent cancer therapies can cause aggressive small cell neuroendocrine carcinoma (SCNC). Researchers found common drivers reprogramming normal cells to SCNC, suggesting shared vulnerabilities for new drug development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Advanced cancer therapies targeting oncogenic pathways can induce resistance, leading to aggressive small cell neuroendocrine carcinoma (SCNC).
  • SCNC presents a poor prognosis due to limited understanding of its molecular drivers and lack of effective treatments.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying SCNC development.
  • To identify shared vulnerabilities in SCNC arising from different epithelial tissues.

Main Methods:

  • Reprogramming of normal human prostate and lung epithelial cells using defined oncogenic drivers.
  • Integrative analysis of epigenetic and transcriptional landscapes in reprogrammed cells.
  • Identification of shared active transcription factor binding regions.

Main Results:

  • Defined oncogenic drivers reproducibly reprogrammed normal prostate and lung epithelial cells into small cell prostate cancer (SCPC) and small cell lung cancer (SCLC), respectively.
  • Shared active transcription factor binding regions were identified in both reprogrammed SCPC and SCLC.
  • These findings indicate common molecular underpinnings in SCNCs derived from distinct tissues.

Conclusions:

  • SCNCs originating from different epithelial tissues may share common vulnerabilities.
  • These shared vulnerabilities could be therapeutically targeted for novel SCNC drug development.

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