Glycidamide promotes the growth and migratory ability of prostate cancer cells by changing the protein expression of cell cycle regulators and epithelial-to-mesenchymal transition (EMT)- associated proteins with prognostic relevance

Titus Ime Ekanem, Chi Chen Huang, Ming Heng Wu, Ding Yen Lin, Wen Fu T. Lai, Kuen Haur Lee

Research output: Contribution to journalArticle

Abstract

Acrylamide (AA) and glycidamide (GA) can be produced in carbohydrate-rich food when heated at a high temperature, which can induce a malignant transformation. It has been demonstrated that GA is more mutagenic than AA. It has been shown that the proliferation rate of some cancer cells are increased by treatment with GA; however, the exact genes that are induced by GA in most cancer cells are not clear. In the present study, we demonstrated that GA promotes the growth of prostate cancer cells through induced protein expression of the cell cycle regulator. In addition, we also found that GA promoted the migratory ability of prostate cancer cells through induced epithelial-to-mesenchymal transition (EMT)-associated protein expression. In order to understand the potential prognostic relevance of GA-mediated regulators of the cell cycle and EMT, we present a three-gene signature to evaluate the prognosis of prostate cancer patients. Further investigations suggested that the three-gene signature (CDK4, TWIST1 and SNAI2) predicted the chances of survival better than any of the three genes alone for the first time. In conclusion, we suggested that the three-gene signature model can act as marker of GA exposure. Hence, this multigene panel may serve as a promising outcome predictor and potential therapeutic target in prostate cancer patients.

Original languageEnglish
Article number2199
JournalInternational Journal of Molecular Sciences
Volume20
Issue number9
DOIs
Publication statusPublished - May 1 2019

Fingerprint

Cell Cycle Proteins
Epithelial-Mesenchymal Transition
regulators
Prostatic Neoplasms
genes
cancer
Cells
proteins
Proteins
Genes
cycles
Growth
signatures
Acrylamide
prognosis
carbohydrates
Carbohydrates
food
markers
glycidamide

Keywords

  • Cell cycle regulator
  • Emt
  • Gene signature
  • Glycidamide
  • Prognosis
  • Prostate cancer

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

Cite this

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title = "Glycidamide promotes the growth and migratory ability of prostate cancer cells by changing the protein expression of cell cycle regulators and epithelial-to-mesenchymal transition (EMT)- associated proteins with prognostic relevance",
abstract = "Acrylamide (AA) and glycidamide (GA) can be produced in carbohydrate-rich food when heated at a high temperature, which can induce a malignant transformation. It has been demonstrated that GA is more mutagenic than AA. It has been shown that the proliferation rate of some cancer cells are increased by treatment with GA; however, the exact genes that are induced by GA in most cancer cells are not clear. In the present study, we demonstrated that GA promotes the growth of prostate cancer cells through induced protein expression of the cell cycle regulator. In addition, we also found that GA promoted the migratory ability of prostate cancer cells through induced epithelial-to-mesenchymal transition (EMT)-associated protein expression. In order to understand the potential prognostic relevance of GA-mediated regulators of the cell cycle and EMT, we present a three-gene signature to evaluate the prognosis of prostate cancer patients. Further investigations suggested that the three-gene signature (CDK4, TWIST1 and SNAI2) predicted the chances of survival better than any of the three genes alone for the first time. In conclusion, we suggested that the three-gene signature model can act as marker of GA exposure. Hence, this multigene panel may serve as a promising outcome predictor and potential therapeutic target in prostate cancer patients.",
keywords = "Cell cycle regulator, Emt, Gene signature, Glycidamide, Prognosis, Prostate cancer",
author = "Ekanem, {Titus Ime} and Huang, {Chi Chen} and Wu, {Ming Heng} and Lin, {Ding Yen} and Lai, {Wen Fu T.} and Lee, {Kuen Haur}",
year = "2019",
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T1 - Glycidamide promotes the growth and migratory ability of prostate cancer cells by changing the protein expression of cell cycle regulators and epithelial-to-mesenchymal transition (EMT)- associated proteins with prognostic relevance

AU - Ekanem, Titus Ime

AU - Huang, Chi Chen

AU - Wu, Ming Heng

AU - Lin, Ding Yen

AU - Lai, Wen Fu T.

AU - Lee, Kuen Haur

PY - 2019/5/1

Y1 - 2019/5/1

N2 - Acrylamide (AA) and glycidamide (GA) can be produced in carbohydrate-rich food when heated at a high temperature, which can induce a malignant transformation. It has been demonstrated that GA is more mutagenic than AA. It has been shown that the proliferation rate of some cancer cells are increased by treatment with GA; however, the exact genes that are induced by GA in most cancer cells are not clear. In the present study, we demonstrated that GA promotes the growth of prostate cancer cells through induced protein expression of the cell cycle regulator. In addition, we also found that GA promoted the migratory ability of prostate cancer cells through induced epithelial-to-mesenchymal transition (EMT)-associated protein expression. In order to understand the potential prognostic relevance of GA-mediated regulators of the cell cycle and EMT, we present a three-gene signature to evaluate the prognosis of prostate cancer patients. Further investigations suggested that the three-gene signature (CDK4, TWIST1 and SNAI2) predicted the chances of survival better than any of the three genes alone for the first time. In conclusion, we suggested that the three-gene signature model can act as marker of GA exposure. Hence, this multigene panel may serve as a promising outcome predictor and potential therapeutic target in prostate cancer patients.

AB - Acrylamide (AA) and glycidamide (GA) can be produced in carbohydrate-rich food when heated at a high temperature, which can induce a malignant transformation. It has been demonstrated that GA is more mutagenic than AA. It has been shown that the proliferation rate of some cancer cells are increased by treatment with GA; however, the exact genes that are induced by GA in most cancer cells are not clear. In the present study, we demonstrated that GA promotes the growth of prostate cancer cells through induced protein expression of the cell cycle regulator. In addition, we also found that GA promoted the migratory ability of prostate cancer cells through induced epithelial-to-mesenchymal transition (EMT)-associated protein expression. In order to understand the potential prognostic relevance of GA-mediated regulators of the cell cycle and EMT, we present a three-gene signature to evaluate the prognosis of prostate cancer patients. Further investigations suggested that the three-gene signature (CDK4, TWIST1 and SNAI2) predicted the chances of survival better than any of the three genes alone for the first time. In conclusion, we suggested that the three-gene signature model can act as marker of GA exposure. Hence, this multigene panel may serve as a promising outcome predictor and potential therapeutic target in prostate cancer patients.

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