Journal
NATURE COMMUNICATIONS
Volume 11, Issue 1, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-020-17492-y
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Funding
- National Natural Science Foundation of China [81725015, 21675098, 21927802]
- Medical and Health Technology Innovation Project of Chinese Academy of Medical Sciences [2016-I2M-3-019, 2016-I2M-4-002, 2019-I2M-2-001]
- Beijing Outstanding Young Scientist Program [BJJWZYJH01201910023027]
- 2018 Beijing Brain Initiative [Z181100001518004]
- Beijing Advanced Innovation Center for Genomics
- Beijing Advanced Innovation Center for Structural Biology
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Esophageal squamous cell carcinoma (ESCC) is prevalent in some geographical regions of the world. ESCC development presents a multistep pathogenic process from inflammation to invasive cancer; however, what is critical in these processes and how they evolve is largely unknown, obstructing early diagnosis and effective treatment. Here, we create a mouse model mimicking human ESCC development and construct a single-cell ESCC developmental atlas. We identify a set of key transitional signatures associated with oncogenic evolution of epithelial cells and depict the landmark dynamic tumorigenic trajectories. An early downregulation of CD8(+) response against the initial tissue damage accompanied by the transition of immune response from type 1 to type 3 results in accumulation and activation of macrophages and neutrophils, which may create a chronic inflammatory environment that promotes carcinogen-transformed epithelial cell survival and proliferation. These findings shed light on how ESCC is initiated and developed. The multistep processes involved in the evolution of inflammation to invasive esophageal squamous cell carcinoma (ESCC) is unclear. Here, the authors report a mouse model of ESCC and the role of interplay between carcinogen-transformed epithelial cells and their microenvironment in ESCC development.
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