Nicotinamide suppresses cell growth by G1-phase arrest and induces apoptosis in intrahepatic cholangiocarcinoma

Yue Wang, Han Suk Ryu, Ja June Jang

Research output: Contribution to journalArticle

Abstract

Intrahepatic cholangiocarcinoma (iCCA) is a devastating malignancy with no effective treatment. Nicotinamide (NA, the amide form of vitamin B3) has been shown to be effective in the treatment of various diseases. However, the effects of NA in iCCA have not been studied. In this study, four human iCCA cell lines (HuCCT1, JCK, OZ and Cho-CK) were used. We found that NA significantly inhibited cell viability and induced apoptosis in vitro. It arrested cell cycle in G1 phase, decreased Cyclin D1 and Cdk4 protein expression levels and increased p16 level. NA increased the levels of cleaved caspases 3 and 9, but had no effect on caspase 8. In HuCCT1 and OZ cell lines, NA treatment significantly impaired the invasion abilities and supressed epithelial-mesenchymal transition (EMT)- like changes. In conclusion, our findings provide the experimental basis for using NA as a potential anticancer agent against human iCCA in the future.

Original languageEnglish
Pages (from-to)43-51
Number of pages9
JournalMolecular and Cellular Toxicology
Volume14
Issue number1
DOIs
StatePublished - 1 Jan 2018

Fingerprint

Niacinamide
Cholangiocarcinoma
G1 Phase
Cell growth
Cells
Apoptosis
Growth
Cyclin-Dependent Kinase 4
Cell Line
Epithelial-Mesenchymal Transition
Caspase 9
Caspase 8
Cyclin D1
Amides
Caspase 3
Antineoplastic Agents
Cell Survival
Cell Cycle
Neoplasms

Keywords

  • Apoptosis
  • Cell Cycle
  • Cholangiocarcinoma
  • Invasion
  • Nicotinamide

Cite this

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abstract = "Intrahepatic cholangiocarcinoma (iCCA) is a devastating malignancy with no effective treatment. Nicotinamide (NA, the amide form of vitamin B3) has been shown to be effective in the treatment of various diseases. However, the effects of NA in iCCA have not been studied. In this study, four human iCCA cell lines (HuCCT1, JCK, OZ and Cho-CK) were used. We found that NA significantly inhibited cell viability and induced apoptosis in vitro. It arrested cell cycle in G1 phase, decreased Cyclin D1 and Cdk4 protein expression levels and increased p16 level. NA increased the levels of cleaved caspases 3 and 9, but had no effect on caspase 8. In HuCCT1 and OZ cell lines, NA treatment significantly impaired the invasion abilities and supressed epithelial-mesenchymal transition (EMT)- like changes. In conclusion, our findings provide the experimental basis for using NA as a potential anticancer agent against human iCCA in the future.",
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Nicotinamide suppresses cell growth by G1-phase arrest and induces apoptosis in intrahepatic cholangiocarcinoma. / Wang, Yue; Ryu, Han Suk; Jang, Ja June.

In: Molecular and Cellular Toxicology, Vol. 14, No. 1, 01.01.2018, p. 43-51.

Research output: Contribution to journalArticle

TY - JOUR

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AU - Wang, Yue

AU - Ryu, Han Suk

AU - Jang, Ja June

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Intrahepatic cholangiocarcinoma (iCCA) is a devastating malignancy with no effective treatment. Nicotinamide (NA, the amide form of vitamin B3) has been shown to be effective in the treatment of various diseases. However, the effects of NA in iCCA have not been studied. In this study, four human iCCA cell lines (HuCCT1, JCK, OZ and Cho-CK) were used. We found that NA significantly inhibited cell viability and induced apoptosis in vitro. It arrested cell cycle in G1 phase, decreased Cyclin D1 and Cdk4 protein expression levels and increased p16 level. NA increased the levels of cleaved caspases 3 and 9, but had no effect on caspase 8. In HuCCT1 and OZ cell lines, NA treatment significantly impaired the invasion abilities and supressed epithelial-mesenchymal transition (EMT)- like changes. In conclusion, our findings provide the experimental basis for using NA as a potential anticancer agent against human iCCA in the future.

AB - Intrahepatic cholangiocarcinoma (iCCA) is a devastating malignancy with no effective treatment. Nicotinamide (NA, the amide form of vitamin B3) has been shown to be effective in the treatment of various diseases. However, the effects of NA in iCCA have not been studied. In this study, four human iCCA cell lines (HuCCT1, JCK, OZ and Cho-CK) were used. We found that NA significantly inhibited cell viability and induced apoptosis in vitro. It arrested cell cycle in G1 phase, decreased Cyclin D1 and Cdk4 protein expression levels and increased p16 level. NA increased the levels of cleaved caspases 3 and 9, but had no effect on caspase 8. In HuCCT1 and OZ cell lines, NA treatment significantly impaired the invasion abilities and supressed epithelial-mesenchymal transition (EMT)- like changes. In conclusion, our findings provide the experimental basis for using NA as a potential anticancer agent against human iCCA in the future.

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