ITCH is a putative target for a novel 20q11.22 amplification detected in anaplastic thyroid carcinoma cells by array-based comparative genomic hybridization

Takaya Ishihara, Hitoshi Tsuda, Akiko Hotta, Ken Ichi Kozaki, Akira Yoshida, Jaeduk Yoshimura Noh, Koichi Ito, Issei Imoto, Johji Inazawa

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Anaplastic thyroid carcinoma (ATC) is one of the most virulent of all human malignancies, with a mean survival time among patients of less than 1 year after diagnosis. To date, however, cytogenetic information on this disease has been very limited. During the course of a program to screen a panel of ATC cell lines for genomic copy-number aberrations using array-based comparative genomic hybridization, we identified a high-level amplification of the ITCH gene, which is mapped to 20q11.22 and belongs to the homologous to the E6-associated protein carboxylterminus ubiquitin ligase family. The expression of ITCH was increased in 4 of 14 ATC cell lines (28.6%), including 8305C in which there was a copy-number amplification of this gene, and six of seven primary cases (85.7%). Among the primary thyroid tumors, a considerable number of ITCH high expressers was found in ATC (40/45, 88.9%), papillary thyroid carcinoma (25/25, 100%), and papillary microcarcinoma (25/25, 100%). Furthermore, knockdown of ITCH by specific small interfering RNA significantly inhibited the growth of ITCH-overexpressing cells, whereas ectopic overexpression of ITCH promoted growth of ATC cell lines with relatively weak expression. These observations indicate ITCH to be the most likely target for 20q11.22 amplification and to play a crucial role in the progression of thyroid carcinoma.

Original languageEnglish
Pages (from-to)1940-1949
Number of pages10
JournalCancer Science
Volume99
Issue number10
DOIs
Publication statusPublished - 2008
Externally publishedYes

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Comparative Genomic Hybridization
Cell Line
Ubiquitin-Protein Ligases
Gene Dosage
Gene Amplification
Growth
Thyroid Neoplasms
Cytogenetics
Small Interfering RNA
Neoplasms
Thyroid Gland
Survival Rate
Anaplastic Thyroid Carcinoma

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

ITCH is a putative target for a novel 20q11.22 amplification detected in anaplastic thyroid carcinoma cells by array-based comparative genomic hybridization. / Ishihara, Takaya; Tsuda, Hitoshi; Hotta, Akiko; Kozaki, Ken Ichi; Yoshida, Akira; Noh, Jaeduk Yoshimura; Ito, Koichi; Imoto, Issei; Inazawa, Johji.

In: Cancer Science, Vol. 99, No. 10, 2008, p. 1940-1949.

Research output: Contribution to journalArticle

Ishihara, Takaya ; Tsuda, Hitoshi ; Hotta, Akiko ; Kozaki, Ken Ichi ; Yoshida, Akira ; Noh, Jaeduk Yoshimura ; Ito, Koichi ; Imoto, Issei ; Inazawa, Johji. / ITCH is a putative target for a novel 20q11.22 amplification detected in anaplastic thyroid carcinoma cells by array-based comparative genomic hybridization. In: Cancer Science. 2008 ; Vol. 99, No. 10. pp. 1940-1949.
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abstract = "Anaplastic thyroid carcinoma (ATC) is one of the most virulent of all human malignancies, with a mean survival time among patients of less than 1 year after diagnosis. To date, however, cytogenetic information on this disease has been very limited. During the course of a program to screen a panel of ATC cell lines for genomic copy-number aberrations using array-based comparative genomic hybridization, we identified a high-level amplification of the ITCH gene, which is mapped to 20q11.22 and belongs to the homologous to the E6-associated protein carboxylterminus ubiquitin ligase family. The expression of ITCH was increased in 4 of 14 ATC cell lines (28.6{\%}), including 8305C in which there was a copy-number amplification of this gene, and six of seven primary cases (85.7{\%}). Among the primary thyroid tumors, a considerable number of ITCH high expressers was found in ATC (40/45, 88.9{\%}), papillary thyroid carcinoma (25/25, 100{\%}), and papillary microcarcinoma (25/25, 100{\%}). Furthermore, knockdown of ITCH by specific small interfering RNA significantly inhibited the growth of ITCH-overexpressing cells, whereas ectopic overexpression of ITCH promoted growth of ATC cell lines with relatively weak expression. These observations indicate ITCH to be the most likely target for 20q11.22 amplification and to play a crucial role in the progression of thyroid carcinoma.",
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