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KRAS(G12D) drives lepidic adenocarcinoma through stem-cell reprogramming.

Nicholas H Juul1,2, Jung-Ki Yoon1,2, Marina C Martinez2

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Researchers discovered that differentiated AT1 cells can reprogram into lung adenocarcinoma stem cells, challenging previous understanding of cancer origins. This finding highlights the critical role of the cell of origin in cancer development.

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Area of Science:

  • Oncology
  • Cell Biology
  • Cancer Stem Cells

Background:

  • Cancers often arise from stem or progenitor cells acquiring mutations.
  • Pulmonary alveolar epithelial type II (AT2) cells are a known cell of origin for lung adenocarcinoma.
  • The role of differentiated cells as cancer origins is less understood.

Purpose of the Study:

  • To investigate the potential of differentiated cells as a source of lung adenocarcinoma.
  • To explore the reprogramming capacity of oncogenic KRAS in differentiated lung cells.
  • To understand the influence of cell of origin on tumor behavior and histology.

Main Methods:

  • Expression of KRAS(G12D) in differentiated AT1 cells in a mouse model.
  • Analysis of cell reprogramming, tumor formation, and progression.
  • Assessment of ERK and WNT pathway activation in response to oncogenic drivers.

Main Results:

  • Differentiated AT1 cells can be reprogrammed into AT2 stem cells by KRAS(G12D) expression.
  • These reprogrammed cells form indolent lung adenocarcinomas with lepidic features.
  • WNT activation differentially affects AT1- and AT2-derived adenomas; ERK augmentation promotes AT1-derived tumor progression.

Conclusions:

  • AT1 cells represent a novel cell of origin for lung adenocarcinoma, recapitulating lepidic cancer features.
  • Oncogenic KRAS can reprogram differentiated cells back to a stem-like state, initiating tumorigenesis.
  • The cell of origin profoundly influences cancer behavior, irrespective of driver oncogenes.