Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 22 P823

ECE2010 Poster Presentations Thyroid (122 abstracts)

DNA repair genes in the thyroid cell lines and human tumors

Justyna Janik , Karolina Hanusek & Barbara Czarnocka


Department of Biochemistry and Molecular Biology, Medical Center for Postgraduate Education, Warsaw, Poland.


Free radicals and reactive oxygen species (ROS) participate in physiological and pathological processes in the thyroid gland. Oxidative stress caused by ROS is involved in many types of DNA damage that are associated with the initiation or the progression of numerous human cancers including thyroid tumors. One of the most mutagenic products of oxygen radical forming agents is 7,8-dihydro-8-oxoguanine (8-oxoG). The aim of the current study was to investigate expression of OGG1 and XRCC1 genes which belong to BER system and take part in the elimination of 8-oxoG from DNA. We determined OGG1 and XRCC1 expression on both transcript and protein levels in the thyroid cancer cell lines and a series of human thyroid tumors and normal thyroid tissues. We analyzed expression of these genes in the lines derived from papillary carcinomas: BCPAP, ONCO-DG-1, TPC-1; follicular carcinomas:FTC-133, FTC-238, CGTH-W-1, ML-1 and non-differentiated carcinoma – 8505C. The normal human thyroid follicular epithelial cells Nthy-ori 3-1 served as a control. In all, but one cell line OGG1 and XRCC1 mRNA expression was on the level similar to that found in the normal thyroid cell line. Significantly decreased expression of both genes was detected in the TPC-1 cell line. Then, thyroid tumours (42), mostly PTC, and normal thyroid (15), were screened for the expression of above genes. Q-RT-PCR method showed that mRNA expression range was similar in cancer and normal tissues. Although we found that the expression of OGG1 and XRCC1 genes in the thyroid cancer cell lines and human thyroid tumors do not differ from the expression in the normal thyroid, further studies are needed to fully investigate DNA modifications and repair mechanisms in the thyroid tumors development.

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