PRMT1 expression is elevated in head and neck cancer and inhibition of protein arginine methylation by adenosine dialdehyde or PRMT1 knockdown downregulates proliferation and migration of oral cancer cells

Chun Yi Chuang, Chien Ping Chang, Yu Jen Lee, Wei Long Lin, Wen Wei Chang, Jia Sian Wu, Ya Wen Cheng, Huei Lee, Chuan Li

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Protein arginine methylation is a post-translational modification that has been implicated in signal transduction, gene transcription, DNA repair and RNA processing. Overexpression or deregulation of protein arginine methyltransferases (PRMTs) have been reported to be associated with various cancers but have not been studied in head and neck cancer (HNC). We investigated the involvement of the modification in HNC using oral cancer cell lines (SAS, OECM-1 and HSC-3) and an immortalized normal oral cells (S-G). The expression levels of the predominant PRMT1 were generally consistent with the levels of asymmetric dimethylarginine (ADMA), highest in SAS and OECM1, then S-G and low in HSC-3. Upon the treatment with an indirect methyltransferase inhibitor adenosine dialdehyde (AdOx), the ADMA levels in SAS and OECM1, but not that in S-G and HSC-3, decreased significantly. SAS and OECM with high ADMA levels grew faster than HSC-3 and S-G. The growth rate of the fast growing SAS and OECM, but not that of the other two cell lines, decreased significantly upon AdOx treatment. The migration activity of SAS and HSC-3, two cell lines with migration ability also decreased after the AdOx treatment. Immunohistochemical analyses of specimens from typical HNC patients showed strong PRMT1 expression in the tumor cells compared with neighboring normal cells. Knockdown of PRMT1 in SAS cells decreased the levels of PRMT1 and ADMA-containing proteins significantly. These cells showed decreased growth rate, reduced migration activity but increased expression of the epithelial marker E-cadherin. The present study thus provides fundamental background for evaluation of the PRMT1 gene as the therapeutic targets of HNC.

Original languageEnglish
Pages (from-to)1115-1123
Number of pages9
JournalOncology Reports
Volume38
Issue number2
DOIs
Publication statusPublished - Aug 1 2017

Fingerprint

Mouth Neoplasms
Head and Neck Neoplasms
Methylation
Arginine
Down-Regulation
Cell Line
Proteins
Protein-Arginine N-Methyltransferases
Gastrin-Secreting Cells
Methyltransferases
Cadherins
Therapeutics
Post Translational Protein Processing
Growth
DNA Repair
Genes
Signal Transduction
Neoplasms
RNA
N,N-dimethylarginine

Keywords

  • Adenosine dialdehyde
  • Head and neck cancer
  • Migration
  • Oral cancer cells
  • PRMT1
  • Protein arginine methylation

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

PRMT1 expression is elevated in head and neck cancer and inhibition of protein arginine methylation by adenosine dialdehyde or PRMT1 knockdown downregulates proliferation and migration of oral cancer cells. / Chuang, Chun Yi; Chang, Chien Ping; Lee, Yu Jen; Lin, Wei Long; Chang, Wen Wei; Wu, Jia Sian; Cheng, Ya Wen; Lee, Huei; Li, Chuan.

In: Oncology Reports, Vol. 38, No. 2, 01.08.2017, p. 1115-1123.

Research output: Contribution to journalArticle

Chuang, Chun Yi ; Chang, Chien Ping ; Lee, Yu Jen ; Lin, Wei Long ; Chang, Wen Wei ; Wu, Jia Sian ; Cheng, Ya Wen ; Lee, Huei ; Li, Chuan. / PRMT1 expression is elevated in head and neck cancer and inhibition of protein arginine methylation by adenosine dialdehyde or PRMT1 knockdown downregulates proliferation and migration of oral cancer cells. In: Oncology Reports. 2017 ; Vol. 38, No. 2. pp. 1115-1123.
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abstract = "Protein arginine methylation is a post-translational modification that has been implicated in signal transduction, gene transcription, DNA repair and RNA processing. Overexpression or deregulation of protein arginine methyltransferases (PRMTs) have been reported to be associated with various cancers but have not been studied in head and neck cancer (HNC). We investigated the involvement of the modification in HNC using oral cancer cell lines (SAS, OECM-1 and HSC-3) and an immortalized normal oral cells (S-G). The expression levels of the predominant PRMT1 were generally consistent with the levels of asymmetric dimethylarginine (ADMA), highest in SAS and OECM1, then S-G and low in HSC-3. Upon the treatment with an indirect methyltransferase inhibitor adenosine dialdehyde (AdOx), the ADMA levels in SAS and OECM1, but not that in S-G and HSC-3, decreased significantly. SAS and OECM with high ADMA levels grew faster than HSC-3 and S-G. The growth rate of the fast growing SAS and OECM, but not that of the other two cell lines, decreased significantly upon AdOx treatment. The migration activity of SAS and HSC-3, two cell lines with migration ability also decreased after the AdOx treatment. Immunohistochemical analyses of specimens from typical HNC patients showed strong PRMT1 expression in the tumor cells compared with neighboring normal cells. Knockdown of PRMT1 in SAS cells decreased the levels of PRMT1 and ADMA-containing proteins significantly. These cells showed decreased growth rate, reduced migration activity but increased expression of the epithelial marker E-cadherin. The present study thus provides fundamental background for evaluation of the PRMT1 gene as the therapeutic targets of HNC.",
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AU - Chuang, Chun Yi

AU - Chang, Chien Ping

AU - Lee, Yu Jen

AU - Lin, Wei Long

AU - Chang, Wen Wei

AU - Wu, Jia Sian

AU - Cheng, Ya Wen

AU - Lee, Huei

AU - Li, Chuan

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AB - Protein arginine methylation is a post-translational modification that has been implicated in signal transduction, gene transcription, DNA repair and RNA processing. Overexpression or deregulation of protein arginine methyltransferases (PRMTs) have been reported to be associated with various cancers but have not been studied in head and neck cancer (HNC). We investigated the involvement of the modification in HNC using oral cancer cell lines (SAS, OECM-1 and HSC-3) and an immortalized normal oral cells (S-G). The expression levels of the predominant PRMT1 were generally consistent with the levels of asymmetric dimethylarginine (ADMA), highest in SAS and OECM1, then S-G and low in HSC-3. Upon the treatment with an indirect methyltransferase inhibitor adenosine dialdehyde (AdOx), the ADMA levels in SAS and OECM1, but not that in S-G and HSC-3, decreased significantly. SAS and OECM with high ADMA levels grew faster than HSC-3 and S-G. The growth rate of the fast growing SAS and OECM, but not that of the other two cell lines, decreased significantly upon AdOx treatment. The migration activity of SAS and HSC-3, two cell lines with migration ability also decreased after the AdOx treatment. Immunohistochemical analyses of specimens from typical HNC patients showed strong PRMT1 expression in the tumor cells compared with neighboring normal cells. Knockdown of PRMT1 in SAS cells decreased the levels of PRMT1 and ADMA-containing proteins significantly. These cells showed decreased growth rate, reduced migration activity but increased expression of the epithelial marker E-cadherin. The present study thus provides fundamental background for evaluation of the PRMT1 gene as the therapeutic targets of HNC.

KW - Adenosine dialdehyde

KW - Head and neck cancer

KW - Migration

KW - Oral cancer cells

KW - PRMT1

KW - Protein arginine methylation

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