SDF1/CXCL12 is involved in recruitment of stem-like progenitor cells to orthotopic murine malignant mesothelioma spheroids

Bonnie Lau, Agnes B. Kane

Research output: Contribution to journalArticle

Abstract

Background/Aim: Tumor progression is influenced by the microenvironment. We found stem cells are recruited to malignant mesothelioma spheroids. We aimed to determine if stem cell recruitment depends on the chemokine SDFl, and if inhibition of the cognate receptor CXCR4 affects tumor growth. Materials and Methods: The kinetics of stem cell recruitment was determined using immunofluorescence staining, BrdU incorporation and eGFP transgenic mice. Chemokines were identified using PCR array. Inhibitors of CXCR4 were used to determine the effect on cell migration and tumor progression. Results: The increasing number of stem cells found in tumor spheroids over time is attributed to cell recruitment. Stem cell migration in vitro was enhanced by exogenous SDF1 and abrogated by CXCR4 inhibition and. CXCR4 inhibition reduced tumor burden in vivo. Conclusion: SDF1 is a candidate chemokine for recruitment of stem cells to malignant peritoneal mesothelioma and a potential target for therapy.

Original languageEnglish (US)
Pages (from-to)2153-2160
Number of pages8
JournalAnticancer Research
Volume30
Issue number6
StatePublished - Jun 1 2010
Externally publishedYes

Fingerprint

Stem Cells
Chemokines
Cell Movement
Neoplasms
CXCR4 Receptors
Bromodeoxyuridine
Tumor Burden
Transgenic Mice
Fluorescent Antibody Technique
Malignant Mesothelioma
Staining and Labeling
Polymerase Chain Reaction
Growth
Therapeutics

Keywords

  • Animal tumor model
  • Chemokine
  • Malignant mesothelioma
  • Mesenchymal stem cell
  • Tumor spheroids

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

SDF1/CXCL12 is involved in recruitment of stem-like progenitor cells to orthotopic murine malignant mesothelioma spheroids. / Lau, Bonnie; Kane, Agnes B.

In: Anticancer Research, Vol. 30, No. 6, 01.06.2010, p. 2153-2160.

Research output: Contribution to journalArticle

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