Metastatic Latency and Immune Evasion through Autocrine Inhibition of WNT
Open accessAbstract
Metastasis frequently develops years after the removal of a primary tumor, from a minority of disseminated cancer cells that survived as latent entities through unknown mechanisms. We isolated latency competent cancer (LCC) cells from early stage human lung and breast carcinoma cell lines and defined the mechanisms that suppress outgrowth, support long-term survival, and maintain tumor-initiating potential in these cells during the latent metastasis stage. LCC cells show stem-cell-like characteristics and express SOX2 and SOX9 transcription factors, which are essential for their survival in host organs under immune surveillance and for metastatic outgrowth under permissive conditions. Through expression of the WNT inhibitor DKK1, LCC cells self-impose a slow-cycling state with broad downregulation of ULBP ligands for NK cells and evasion of NK-cell-mediated clearance. By expressing a Sox-dependent stem-like state and actively silencing WNT signaling, LCC cells can enter quiescence and evade innate immunity to remain latent for extended periods.
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In vivo selection identified latency-competent cancer cells that exhibited a quiescent-like state resembling stem and progenitor cells.
“When in vivo selection was used to identify latency-competent cancer cells, these tumors exhibited a quiescent-like state reminiscent of stem and progenitor cells (102).”
From Metabolic reprogramming and cancer progression (2020) · cites this paper as [102]
In a mouse LUAD model carrying compound EgfrL858R/T790M mutations, Ctnnb1 deletion lowered tumor burden, which suggests non-redundant roles in initiating tumors.
“in a mouse LUAD model driven by compound EgfrL858R/T790M mutations genetic deletion of Ctnnb1 reduced tumor burden indicating non-redundant functions in tumor initiation122”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [122]
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- Authors
- Malladi, S., Macalinao, D. G., Jin, X., He, L., Basnet, H., Zou, Y., de Stanchina, E., & Massagué, J.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Massagué, Joan
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2016-03
- Volume
- 165
- Issue
- 1
- Pages
- 45-60
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4808520
- OpenAlex
- W2303309927
- Cited by
- 791
- References
- 60
- Citations by year
- 2026: 51 · 2025: 85 · 2024: 84 · 2023: 90 · 2022: 76 · 2021: 101 · 2020: 86 · 2019: 76 · 2018: 60 · 2017: 55 · 2016: 25 · 2015: 1
- FWCI
- 38.78
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Memorial Sloan Kettering Cancer Center
- NIH (P01-CA094060, P01-CA129243, P30-CA008748)
- DOD (W81XWH-12-1-0074)
- American Cancer Society post-doctoral fellowship
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
- Keywords
- metastatic latency, immune evasion, Wnt signaling inhibition, DKK1, SOX2, SOX9, cancer stem cells, NK cell evasion, quiescence, lung cancer, breast cancer, innate immunity
- MeSH terms
- Animals, Breast Neoplasms, Female, Humans, Immunologic Surveillance, Killer Cells, Natural, Lung Neoplasms, Mice, Nude, Neoplasm Metastasis, Tumor Escape, Autocrine Communication, Intercellular Signaling Peptides and Proteins, Cell Line, Tumor, Mice, SOXB1 Transcription Factors, SOX9 Transcription Factor, Wnt Signaling Pathway
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