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[Transmembrane controls in cultured human thyroid carcinoma].

Y Abe1

  • 1Department of Internal Medicine Kitasato University, School of Medicine, Sagamihara, Japan.

Human Cell
|September 1, 1989
PubMed
Summary

Thyroid carcinoma cells show altered responsiveness to thyroid-stimulating hormone (TSH), with increased adenylate cyclase activity and changes in desensitization potentially linked to neoplastic growth.

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Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Thyroid carcinoma often retains some responsiveness to thyroid-stimulating hormone (TSH).
  • Alterations in TSH signaling pathways may contribute to thyroid cancer development and progression.

Purpose of the Study:

  • To investigate the alterations in TSH responsiveness in human thyroid carcinoma.
  • To explore the relationship between TSH signaling, oncogene expression, and receptor function in thyroid cancer.

Main Methods:

  • Western blotting analysis to assess ras oncogene product p21 expression.
  • Measurement of adenylate cyclase responsiveness to TSH in carcinoma and normal thyroid tissue.
  • Evaluation of epidermal growth factor (EGF) receptor capacity and binding in cultured carcinoma cells.

Main Results:

  • Adenylate cyclase responsiveness to TSH was generally greater in thyroid carcinoma than in normal thyroid tissue.
  • Increased adenylate cyclase response correlated with enhanced expression of ras oncogene product p21.
  • TSH-induced desensitization of adenylate cyclase was absent in some differentiated carcinomas, possibly due to altered ADP-ribosylable Gi protein.
  • Epidermal growth factor receptor capacity was higher in differentiated carcinoma cells, but EGF binding did not increase with TSH stimulation.

Conclusions:

  • Altered transmembrane signaling, including TSH responsiveness and EGF receptor function, may play a role in the neoplastic growth of human thyroid carcinoma.
  • Specific molecular changes, such as altered Gi protein function and oncogene expression, contribute to the aberrant TSH signaling observed in thyroid cancer.

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