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Inhibition of endogenous SPARC enhances pancreatic cancer cell growth: modulation by FGFR1-III isoform expression

G Chen1, X Tian, Z Liu

  • 1Clinic of General, Visceral, and Transplantation Surgery, University of Ulm, Steinhoevelstrasse 9, Ulm 89075, Germany.

British Journal of Cancer
|November 19, 2009
PubMed
Abstract

Insights

Secreted protein acidic and rich in cysteine (SPARC) acts as a tumor suppressor in pancreatic ductal adenocarcinoma (PDAC). Its expression is modulated by fibroblast growth factor receptor (FGFR) 1 isoforms and can be suppressed by PDAC cells.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Secreted protein acidic and rich in cysteine (SPARC) influences cell interactions and has a dual role in cancer, potentially acting as a tumor suppressor.
  • Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer where SPARC's function requires further characterization.

Purpose of the Study:

  • To investigate the function of SPARC in PDAC.
  • To determine how fibroblast growth factor receptor (FGFR) 1 isoforms modulate SPARC expression and function in PDAC.

Main Methods:

  • Utilized exogenous SPARC to assess its effects on cell growth and migration.
  • Employed short hairpin RNA (shRNA) to inhibit endogenous SPARC in PDAC cell lines (ASPC-1, PANC-1).
  • Overexpressed FGFR1-IIIb and FGFR1-IIIc isoforms in PANC-1 cells and analyzed SPARC expression changes, including the role of p38-MAPK inhibitor SB203580.

Main Results:

  • Exogenous SPARC inhibited PDAC cell growth, movement, and migration.
  • Inhibition of endogenous SPARC increased anchorage-dependent/independent growth, migration, xenograft growth, and FGF mitogenic efficacy.
  • FGFR1-IIIb overexpression increased endogenous SPARC, while FGFR1-IIIc overexpression decreased it; p38-MAPK inhibition abrogated SPARC upregulation.
  • SPARC was found in pancreatic stellate cell (PSC) conditioned medium, but not PDAC cells; PDAC conditioned medium reduced SPARC expression in PSCs.

Conclusions:

  • Endogenous SPARC functions as a tumor suppressor in PDAC by inhibiting the malignant phenotype.
  • FGFR1-III isoform expression significantly modulates endogenous SPARC levels in PDAC cells.
  • PDAC cells can suppress SPARC expression in surrounding PSCs through paracrine signaling, suggesting complex tumor microenvironment interactions.

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