ArticleLaboratory investigation; a journal of technical methods and pathology2016
Requirement of CXCL12-CXCR7 signaling for CD20(-) CD138(-) double-negative population in lymphoplasmacytic lymphoma.
Article in Laboratory investigation; a journal of technical methods and pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 6 citations in OpenAlex.
- Review
- Plasma cells arise from differentiation of clonal lymphocytes and secrete IgM in Waldenström macroglobulinemia.iScience · 2022Article
- Review
- Heterogeneity of tumor cells in terms of cancer-initiating cells.Journal of toxicologic pathology · 2017Review
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Authors and funding
7 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Cancer cells with tumorigenic potential are limited to a small subpopulation known as cancer-initiating cells (CICs). Recently we investigated a candidate of CICs of lymphoplasmacytic lymphoma (LPL), which is positive for both B-cell marker CD20 and plasma-cell marker CD138. We reported that the subpopulation of CD20(-) CD138(-) phenotype, in which both markers were negative was a candidate of CICs in LPL using LPL cell line, MWCL-1. CICs are known to be plastic under stressed condition, in which non-CICs are changed to CICs. In the present study, we investigated the plasticity of CICs of LPL, and found that hypoxia induced the conversion of CD20(+) CD138(-) to CD20(-) CD138(-) phenotype. We then searched for markers preferentially expressed in CD20(-) CD138(-) subpopulation, and the chemokine receptor CXCR7 was isolated. When cultured with CXCL12, a ligand of CXCR7, the number of CD20(-) CD138(-) cells increased in a time- and dose-dependent manner. In addition, hypoxia enhanced the expression level of CXCL12 in MWCL-1. In clinical samples of LPL, a few tumor cells expressed CXCR7, in which CD20 expression was not detected. These results indicated that hypoxia and CXCL12-CXCR7 axis appeared to be advantageous microenvironments to CD20(-) CD138(-) cells.
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