USF inhibits cell proliferation through delay in G2/M phase in FRTL-5 cells

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Updated: Jul 16, 2026

Analysis of Cell Cycle Position in Mammalian Cells
12:19

Analysis of Cell Cycle Position in Mammalian Cells

Published on: January 21, 2012

Hye Seung Jung1, Keun-Sook Kim, Yun Jae Chung

  • 1Division of Endocrinology and Metabolism, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Korea.

Endocrine Journal
|March 24, 2007
PubMed

Insights

Upstream stimulatory factors (USF-1 and USF-2) inhibit thyroid cell proliferation by delaying the cell cycle. These factors suppress proliferation in normal thyrocytes and thyroid cancer cells while maintaining thyroid stimulating hormone-stimulated cAMP production.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Biology

Background:

  • Upstream stimulatory factor (USF) is known to negatively regulate cell proliferation in various cell types.
  • The specific role of USF in the proliferation and function of thyroid follicular cells remains unclear.

Purpose of the Study:

  • To investigate the effects of USF on the proliferation and function of normal thyrocytes and thyroid carcinoma cells.
  • To elucidate the molecular mechanisms underlying USF's impact on cell cycle regulation in thyroid cells.

Main Methods:

  • Complementary DNAs for USF-1 and USF-2 were synthesized and transfected into FRTL-5 cells and papillary thyroid carcinoma cell lines.
  • Assays included cyclic AMP (cAMP) production, [methyl-3H] thymidine uptake, 5-bromo-2'-deoxyuridine (BrdU) uptake, apoptosis testing (Hoechst staining), cell cycle analysis (FACS), and gene expression analysis (Northern and Western blotting).

Main Results:

  • Overexpression of USF-1 and USF-2 significantly suppressed thyroid stimulating hormone (TSH)-stimulated [methyl-3H] thymidine uptake in FRTL-5 cells but maintained cAMP production.
  • USF overexpression significantly suppressed BrdU uptake in thyroid carcinoma cell lines (NPA and TPC-1), indicating reduced proliferation.
  • USF overexpression induced a delay in the G2/M phase of the cell cycle, decreased cyclin B1 and CDK-1 expression, and increased p27 expression, without increasing apoptosis.

Conclusions:

  • USF-1 and USF-2 suppress the proliferation of both normal thyrocytes and thyroid carcinoma cells.
  • USF overexpression inhibits thyroid cell proliferation partly through a delay in the G2/M phase of the cell cycle.
  • Despite inhibiting proliferation, USF maintains the ability of thyrocytes to produce cAMP in response to TSH stimulation.

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