LKB1/STK11 Inactivation Leads to Expansion of a Prometastatic Tumor Subpopulation in Melanoma
Open accessAbstract
Germline mutations in LKB1 (STK11) are associated with the Peutz-Jeghers syndrome (PJS), which includes aberrant mucocutaneous pigmentation, and somatic LKB1 mutations occur in 10% of cutaneous melanoma. By somatically inactivating Lkb1 with K-Ras activation (±p53 loss) in murine melanocytes, we observed variably pigmented and highly metastatic melanoma with 100% penetrance. LKB1 deficiency resulted in increased phosphorylation of the SRC family kinase (SFK) YES, increased expression of WNT target genes, and expansion of a CD24(+) cell population, which showed increased metastatic behavior in vitro and in vivo relative to isogenic CD24(-) cells. These results suggest that LKB1 inactivation in the context of RAS activation facilitates metastasis by inducing an SFK-dependent expansion of a prometastatic, CD24(+) tumor subpopulation.
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Self-citationLKB1 inhibits HPV-associated cancer progression by targeting cellular metabolism
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YES1 Drives Lung Cancer Growth and Progression and Predicts Sensitivity to Dasatinib
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Targeting the LKB1 Tumor Suppressor
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YES1: A Novel Therapeutic Target and Biomarker in Cancer
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LKB1 and cancer: The dual role of metabolic regulation
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LKB1 loss in melanoma disrupts directional migration toward extracellular matrix cues
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Comparative oncogenomics identifies tyrosine kinase FES as a tumor suppressor in melanoma
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Silencing of CD24 Enhances the PRIMA-1–Induced Restoration of Mutant p53 in Prostate Cancer Cells
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LKB1: Can We Target an Hidden Target? Focus on NSCLC
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LKB1 specifies neural crest cell fates through pyruvate-alanine cycling
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The role of STK11/LKB1 in cancer biology: implications for ovarian tumorigenesis and progression
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Emerging Roles of YES1 in Cancer: The Putative Target in Drug Resistance
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Dependency of human and murine LKB1-inactivated lung cancer on aberrant CRTC-CREB activation
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RetractedThe LKB1 Tumor Suppressor as a Biomarker in Mouse and Human Tissues
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STK11 is required for the normal program of ciliated cell differentiation in airways
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Lkb1 Loss Promotes Tumor Progression of BRAFV600E-Induced Lung Adenomas
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The Genetic Basis of Dormancy and Awakening in Cutaneous Metastatic Melanoma
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Upregulation of liver kinase B1 predicts poor prognosis in hepatocellular carcinoma
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Role of YES1 signaling in tumor therapy resistance
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Intravital imaging of a spheroid-based orthotopic model of melanoma in the mouse ear skin
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Self-citationPrognostic significance of LKB1 promoter methylation in cutaneous malignant melanoma
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mTOR Signaling in Melanoma: Oncogene-Induced Pseudo-Senescence?
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Self-citationSTK11 mutation status is associated with decreased survival in meningiomas
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LKB1 regulates JNK-dependent stress signaling and apoptotic dependency of KRAS-mutant lung cancers
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“Loss of the tumor suppressor STK11/ LKB1 19 facilitates tumorigenesis by modulating energy balance 20,21 , enhancing metastatic potential 22,23 ,andenablingimmuneevasion 9,24 .”
Ultrathin primary is a marker for worse prognosis in lymph node–positive cutaneous melanoma
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Germline mutations in patients with multiple colorectal polyps in China
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A renaissance for YES in cancer
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LKB1 as a Tumor Suppressor in Uterine Cancer: Mouse Models and Translational Studies
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STK11 Loss: A Novel Mechanism for Melanoma Metastasis with Therapeutic Implications
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- Authors
- Liu, W., Monahan, K. B., Pfefferle, A. D., Shimamura, T., Sorrentino, J., Chan, K. T., Roadcap, D. W., Ollila, D. W., Thomas, N. E., Castrillon, D. H., Miller, C. R., Perou, C. M., Wong, K.-K., Bear, J. E., & Sharpless, N. E.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Loyola University Chicago (US)
- Harvard University (US)
- Corresponding author
- Sharpless, Norman E.
- ORCID
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2012-06
- Volume
- 21
- Issue
- 6
- Pages
- 751-764
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC3660964
- OpenAlex
- W1974228534
- Cited by
- 127
- References
- 55
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 6 · 2023: 7 · 2022: 7 · 2021: 7 · 2020: 7 · 2019: 7 · 2018: 8 · 2017: 14 · 2016: 9 · 2015: 15 · 2014: 19 · 2013: 10 · 2012: 4
- FWCI
- 7.59
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 447 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- Minerva Access (University of Melbourne) (submittedVersion)
- UNC Libraries
- Funders
- National Cancer Institute
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- STK11/LKB1, melanoma, metastasis, Src family kinases, Yes kinase, Wnt signaling, KRAS activation, p53 deficiency, Peutz-Jeghers syndrome, melanocyte transformation, tumor heterogeneity
- MeSH terms
- Dasatinib, Animals, Cells, Cultured, Female, Humans, Melanocytes, Melanoma, Mice, Nude, Mutation, Neoplasm Metastasis, Pyrimidines, Thiazoles, Transplantation, Heterologous, Immunoblotting, Gene Expression Regulation, Neoplastic, Tumor Suppressor Protein p53, Proto-Oncogene Proteins p21(ras), Protein Serine-Threonine Kinases, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, RNA Interference, Cell Line, Tumor, Protein Kinase Inhibitors, Cell Proliferation, Mice, Proto-Oncogene Proteins c-yes, CD24 Antigen, AMP-Activated Protein Kinases
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