In thyroid cancer cell lines expression of periostin gene is controlled by p73 and is not related to epigenetic marks of active transcription

Cinzia Puppin, Nadia Passon, Francesco Frasca, Riccardo Vigneri, Federica Tomay, Stefania Tomaciello, Giuseppe Damante

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Background Periostin expression is a feature of the epithelialmesenchymal transition, which occurs during cancer progression. Previous reports indicate that periostin expression is related to tumour aggressiveness. Methods In order to identify mechanisms regulating periostin expression in thyroid cancer, a panel of continuous thyroid cancer cell lines was investigated. Levels of posttranslational modifications of the H3 histone were investigated by chromatin immunoprecipitation. Moreover, treatment of cell lines with deacetylase inhibitors and transfection experiments were performed. Results Our insights show that levels of H3 histone acetylated at lysines 9 and 14 (which are epigenetic marks of active transcription) are not related to periostin mRNA levels. Moreover, treatment of WRO and FRO thyroid cancer cell lines with the deacetylase inhibitor tricostatin A (TSA) or suberoylanilide hydroxamic acid (SAHA) increases levels of acetylated H3 histone to periostin promoter however, unpredictably, reduces periostin mRNA levels. Interestingly, treatment of WRO cells with either TSA or SAHA increases levels of the H3 histone trimethylated at lysine 4, which is a different epigenetic mark of active transcription. Instead, data obtained by cell transfection indicate that δNp73, a member of p53 family selectively expressed in thyroid carcinomas, plays a role in activating periostin gene expression. Conclusions Levels of epigenetic marks of active transcription do not contribute to regulation of periostin gene expression. The δNp73 effects suggest a novel molecular mechanism involved in thyroid cancer progression.

Original languageEnglish
Pages (from-to)131-140
Number of pages10
JournalCellular Oncology
Volume34
Issue number2
DOIs
Publication statusPublished - Apr 2011

Fingerprint

Thyroid Neoplasms
Epigenomics
Histones
trichostatin A
Gene Expression
Cell Line
Lysine
Transfection
Messenger RNA
Chromatin Immunoprecipitation
Gene Expression Regulation
Post Translational Protein Processing
Neoplasms
vorinostat

Keywords

  • Gene expression
  • Histone acetylation
  • P73
  • Periostin
  • Thyroid tumours

ASJC Scopus subject areas

  • Cancer Research
  • Molecular Medicine
  • Oncology
  • Medicine(all)

Cite this

In thyroid cancer cell lines expression of periostin gene is controlled by p73 and is not related to epigenetic marks of active transcription. / Puppin, Cinzia; Passon, Nadia; Frasca, Francesco; Vigneri, Riccardo; Tomay, Federica; Tomaciello, Stefania; Damante, Giuseppe.

In: Cellular Oncology, Vol. 34, No. 2, 04.2011, p. 131-140.

Research output: Contribution to journalArticle

Puppin, Cinzia ; Passon, Nadia ; Frasca, Francesco ; Vigneri, Riccardo ; Tomay, Federica ; Tomaciello, Stefania ; Damante, Giuseppe. / In thyroid cancer cell lines expression of periostin gene is controlled by p73 and is not related to epigenetic marks of active transcription. In: Cellular Oncology. 2011 ; Vol. 34, No. 2. pp. 131-140.
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N2 - Background Periostin expression is a feature of the epithelialmesenchymal transition, which occurs during cancer progression. Previous reports indicate that periostin expression is related to tumour aggressiveness. Methods In order to identify mechanisms regulating periostin expression in thyroid cancer, a panel of continuous thyroid cancer cell lines was investigated. Levels of posttranslational modifications of the H3 histone were investigated by chromatin immunoprecipitation. Moreover, treatment of cell lines with deacetylase inhibitors and transfection experiments were performed. Results Our insights show that levels of H3 histone acetylated at lysines 9 and 14 (which are epigenetic marks of active transcription) are not related to periostin mRNA levels. Moreover, treatment of WRO and FRO thyroid cancer cell lines with the deacetylase inhibitor tricostatin A (TSA) or suberoylanilide hydroxamic acid (SAHA) increases levels of acetylated H3 histone to periostin promoter however, unpredictably, reduces periostin mRNA levels. Interestingly, treatment of WRO cells with either TSA or SAHA increases levels of the H3 histone trimethylated at lysine 4, which is a different epigenetic mark of active transcription. Instead, data obtained by cell transfection indicate that δNp73, a member of p53 family selectively expressed in thyroid carcinomas, plays a role in activating periostin gene expression. Conclusions Levels of epigenetic marks of active transcription do not contribute to regulation of periostin gene expression. The δNp73 effects suggest a novel molecular mechanism involved in thyroid cancer progression.

AB - Background Periostin expression is a feature of the epithelialmesenchymal transition, which occurs during cancer progression. Previous reports indicate that periostin expression is related to tumour aggressiveness. Methods In order to identify mechanisms regulating periostin expression in thyroid cancer, a panel of continuous thyroid cancer cell lines was investigated. Levels of posttranslational modifications of the H3 histone were investigated by chromatin immunoprecipitation. Moreover, treatment of cell lines with deacetylase inhibitors and transfection experiments were performed. Results Our insights show that levels of H3 histone acetylated at lysines 9 and 14 (which are epigenetic marks of active transcription) are not related to periostin mRNA levels. Moreover, treatment of WRO and FRO thyroid cancer cell lines with the deacetylase inhibitor tricostatin A (TSA) or suberoylanilide hydroxamic acid (SAHA) increases levels of acetylated H3 histone to periostin promoter however, unpredictably, reduces periostin mRNA levels. Interestingly, treatment of WRO cells with either TSA or SAHA increases levels of the H3 histone trimethylated at lysine 4, which is a different epigenetic mark of active transcription. Instead, data obtained by cell transfection indicate that δNp73, a member of p53 family selectively expressed in thyroid carcinomas, plays a role in activating periostin gene expression. Conclusions Levels of epigenetic marks of active transcription do not contribute to regulation of periostin gene expression. The δNp73 effects suggest a novel molecular mechanism involved in thyroid cancer progression.

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