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Transforming growth factor-beta is an endogenous radioresistance factor in the esophageal adenocarcinoma cell line

Albert H Kim1, Deborah A Lebman, Christopher M Dietz

  • 1Department of Radiation Oncology, Massey Cancer Center and Medical College of Virginia at Virginia Commonwealth University, Richmond, VA 23298-0058, USA.

International Journal of Oncology
|November 13, 2003
PubMed

Insights

Transforming growth factor-beta (TGF-β) enhances radioresistance in OE-33 esophageal cancer cells by inducing cell cycle arrest. This suggests TGF-β acts as an endogenous factor that increases cancer cell survival after radiation exposure.

Area of Science:

  • Oncology
  • Cell Biology
  • Radiation Biology

Background:

  • Transforming growth factor-beta (TGF-β) influences epithelial cell differentiation and radiation response.
  • Previous studies showed TGF-β downregulates c-myc mRNA and inhibits OE-33 cell growth.
  • The role of TGF-β in esophageal cancer cell radiosensitivity requires further investigation.

Purpose of the Study:

  • To investigate the role of TGF-β in the in vitro radiation response of OE-33 and other esophageal cancer cell lines.
  • To determine if TGF-β confers radioresistance in different types of esophageal cancer cells.
  • To elucidate the mechanisms underlying TGF-β-mediated radioresistance.

Main Methods:

  • Exposure of five human esophageal cancer cell lines (OE-33, BIC1, SEG1, KYSE, OE-21) to ionizing radiation with and without TGF-β.
  • Analysis of cell cycle distribution and expression of p27kip1 and c-myc protein.
  • Assessment of radiosensitivity using surviving fraction at 2 Gy (SF2).
  • Evaluation of conditioned medium from OE-33 cells and neutralization with anti-TGF-β antibodies.
  • Measurement of TGF-β production using enzyme-linked immunoabsorbent assays (ELISA) after radiation exposure.

Main Results:

  • TGF-β enhanced radioresistance in OE-33 cells but not in BIC1, SEG1, KYSE, or OE-21 cells.
  • TGF-β-induced radioresistance in OE-33 cells was linked to G0/G1 cell cycle arrest and p27kip1 upregulation, with c-myc downregulation.
  • OE-33 cells exhibited inherent radioresistance compared to BIC1 and SEG1 cells.
  • Endogenous TGF-β produced by OE-33 cells contributed to radioresistance, as indicated by conditioned medium experiments.
  • Ionizing radiation increased TGF-β production in all tested cell lines.

Conclusions:

  • TGF-β acts as an endogenous, radiation-inducible radioresistance factor specifically in OE-33 esophageal carcinoma cells.
  • The findings highlight a potential therapeutic target for overcoming radioresistance in certain esophageal cancers.
  • Differential responses among cell lines suggest TGF-β's role in radioresistance is context-dependent.

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