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Published on: June 16, 2018
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Selectins mediate small cell lung cancer systemic metastasis.
Franziska Heidemann1, Anna Schildt1, Katharina Schmid2
1Department of Anatomy and Experimental Morphology, University Medical Center Hamburg- Eppendorf, Hamburg, Germany.
Plos One
|April 5, 2014
Summary
Small cell lung cancer (SCLC) cells use selectin adhesion molecules to metastasize. Blocking E- and P-selectin reduced metastasis by 50%, suggesting these molecules are key drivers of SCLC spread.
Area of Science:
- Oncology
- Cell Biology
- Molecular Biology
Background:
- Metastasis formation significantly worsens prognosis for small cell lung cancer (SCLC) patients.
- Molecular mechanisms driving SCLC metastasis are largely unknown.
- Tumor cells can hijack leukocyte adhesion pathways to facilitate metastasis.
Purpose of the Study:
- To investigate the role of selectin-mediated adhesion in SCLC metastasis.
- To identify molecular partners involved in SCLC cell adhesion and metastasis.
Main Methods:
- Utilized the human OH-1 SCLC cell line as a model.
- Analyzed E- and P-selectin binding sites and associated glycotopes (sialyl Lewis A).
- Detected selectin ligand proteins (PSGL-1, CD44, CEA) in SCLC cells.
- Performed intravital microscopy in mice to observe SCLC cell rolling.
- Xenografted OH-1 cells into wild-type and E-/P-selectin-deficient mice.
Main Results:
- OH-1 SCLC cells express E- and P-selectin binding sites, partly due to sialyl Lewis A.
- SCLC cells exhibit leukocyte-like rolling behavior on murine mesenteric vasculature.
- Xenografting into E-/P-selectin-deficient mice reduced spontaneous metastasis by 50% (p=0.0181).
Conclusions:
- SCLC cells utilize selectin-mediated adhesion, mimicking leukocyte rolling, to initiate metastasis.
- The E-/P-selectin pathway is a significant contributor to SCLC metastasis.
- Redundancy within the adhesion cascade suggests other molecules also mediate metastasis, contributing to SCLC's high metastatic potential.
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