Mechanism of β-carotene-induced apoptosis of gastric cancer cells: Involvement of ataxia-telangiectasia-mutated

Sung Hee Jang, Joo Weon Lim, Hye Young Kim

Research output: Chapter in Book/Report/Conference proceedingConference contribution

16 Citations (Scopus)

Abstract

β-Carotene acts as an antioxidant or a pro-oxidant depending on the concentrations that cells are treated with. Oxidative DNA damage is related to apoptosis of various cells. Ataxia-telangiectasia-mutated (ATM), a sensor for DNA-damaging agents, activates a variety of effectors in multiple signaling pathways, such as DNA repair and apoptosis. In the present study, we investigated whether a high concentration of β-carotene induces apoptosis of gastric adenocarcinoma (AGS) cells and whether ATM is involved in β-carotene-induced apoptosis of AGS cells. We found that β-carotene (100 μmol/L) induced apoptosis (determined by cell viability), DNA fragmentation, and the protein levels of p53 and Bcl-2 in AGS cells. ATM levels in the nucleus decreased from β-carotene in AGS cells. β-Carotene- induced alterations, including an increase in DNA fragmentation and p53 levels and a decrease in nuclear ATM and cellular Bcl-2 levels, were inhibited in the cells transfected with full-length ATM cDNA compared to wild-type cells or the cells transfected with control vector plasmid control DNA vector (pcDNA). In conclusion, β-carotene induces apoptosis by increasing apoptotic protein p53 and decreasing anti-apoptotic Bcl-2 as well as nuclear ATM in AGS cells. Nuclear loss of ATM may be the underlying mechanism of β-carotene-induced apoptosis of gastric cancer cells.

Original languageEnglish
Title of host publicationNatural Compounds and Their Role in Apoptotic Cell Signaling Pathways
PublisherBlackwell Publishing Inc.
Pages156-162
Number of pages7
ISBN (Print)9781573317375
DOIs
Publication statusPublished - 2009 Jan 1

Publication series

NameAnnals of the New York Academy of Sciences
Volume1171
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

Fingerprint

Ataxia Telangiectasia
Carotenoids
Stomach Neoplasms
Cells
Apoptosis
Stomach
Adenocarcinoma
DNA
DNA Fragmentation
Cancer
DNA Repair
DNA Damage
Reactive Oxygen Species
Cell Survival
Proteins
Plasmids
Repair
Complementary DNA
Antioxidants

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

Cite this

Jang, S. H., Lim, J. W., & Kim, H. Y. (2009). Mechanism of β-carotene-induced apoptosis of gastric cancer cells: Involvement of ataxia-telangiectasia-mutated. In Natural Compounds and Their Role in Apoptotic Cell Signaling Pathways (pp. 156-162). (Annals of the New York Academy of Sciences; Vol. 1171). Blackwell Publishing Inc.. https://doi.org/10.1111/j.1749-6632.2009.04711.x
Jang, Sung Hee ; Lim, Joo Weon ; Kim, Hye Young. / Mechanism of β-carotene-induced apoptosis of gastric cancer cells : Involvement of ataxia-telangiectasia-mutated. Natural Compounds and Their Role in Apoptotic Cell Signaling Pathways. Blackwell Publishing Inc., 2009. pp. 156-162 (Annals of the New York Academy of Sciences).
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Jang, SH, Lim, JW & Kim, HY 2009, Mechanism of β-carotene-induced apoptosis of gastric cancer cells: Involvement of ataxia-telangiectasia-mutated. in Natural Compounds and Their Role in Apoptotic Cell Signaling Pathways. Annals of the New York Academy of Sciences, vol. 1171, Blackwell Publishing Inc., pp. 156-162. https://doi.org/10.1111/j.1749-6632.2009.04711.x

Mechanism of β-carotene-induced apoptosis of gastric cancer cells : Involvement of ataxia-telangiectasia-mutated. / Jang, Sung Hee; Lim, Joo Weon; Kim, Hye Young.

Natural Compounds and Their Role in Apoptotic Cell Signaling Pathways. Blackwell Publishing Inc., 2009. p. 156-162 (Annals of the New York Academy of Sciences; Vol. 1171).

Research output: Chapter in Book/Report/Conference proceedingConference contribution

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T1 - Mechanism of β-carotene-induced apoptosis of gastric cancer cells

T2 - Involvement of ataxia-telangiectasia-mutated

AU - Jang, Sung Hee

AU - Lim, Joo Weon

AU - Kim, Hye Young

PY - 2009/1/1

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N2 - β-Carotene acts as an antioxidant or a pro-oxidant depending on the concentrations that cells are treated with. Oxidative DNA damage is related to apoptosis of various cells. Ataxia-telangiectasia-mutated (ATM), a sensor for DNA-damaging agents, activates a variety of effectors in multiple signaling pathways, such as DNA repair and apoptosis. In the present study, we investigated whether a high concentration of β-carotene induces apoptosis of gastric adenocarcinoma (AGS) cells and whether ATM is involved in β-carotene-induced apoptosis of AGS cells. We found that β-carotene (100 μmol/L) induced apoptosis (determined by cell viability), DNA fragmentation, and the protein levels of p53 and Bcl-2 in AGS cells. ATM levels in the nucleus decreased from β-carotene in AGS cells. β-Carotene- induced alterations, including an increase in DNA fragmentation and p53 levels and a decrease in nuclear ATM and cellular Bcl-2 levels, were inhibited in the cells transfected with full-length ATM cDNA compared to wild-type cells or the cells transfected with control vector plasmid control DNA vector (pcDNA). In conclusion, β-carotene induces apoptosis by increasing apoptotic protein p53 and decreasing anti-apoptotic Bcl-2 as well as nuclear ATM in AGS cells. Nuclear loss of ATM may be the underlying mechanism of β-carotene-induced apoptosis of gastric cancer cells.

AB - β-Carotene acts as an antioxidant or a pro-oxidant depending on the concentrations that cells are treated with. Oxidative DNA damage is related to apoptosis of various cells. Ataxia-telangiectasia-mutated (ATM), a sensor for DNA-damaging agents, activates a variety of effectors in multiple signaling pathways, such as DNA repair and apoptosis. In the present study, we investigated whether a high concentration of β-carotene induces apoptosis of gastric adenocarcinoma (AGS) cells and whether ATM is involved in β-carotene-induced apoptosis of AGS cells. We found that β-carotene (100 μmol/L) induced apoptosis (determined by cell viability), DNA fragmentation, and the protein levels of p53 and Bcl-2 in AGS cells. ATM levels in the nucleus decreased from β-carotene in AGS cells. β-Carotene- induced alterations, including an increase in DNA fragmentation and p53 levels and a decrease in nuclear ATM and cellular Bcl-2 levels, were inhibited in the cells transfected with full-length ATM cDNA compared to wild-type cells or the cells transfected with control vector plasmid control DNA vector (pcDNA). In conclusion, β-carotene induces apoptosis by increasing apoptotic protein p53 and decreasing anti-apoptotic Bcl-2 as well as nuclear ATM in AGS cells. Nuclear loss of ATM may be the underlying mechanism of β-carotene-induced apoptosis of gastric cancer cells.

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M3 - Conference contribution

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SN - 9781573317375

T3 - Annals of the New York Academy of Sciences

SP - 156

EP - 162

BT - Natural Compounds and Their Role in Apoptotic Cell Signaling Pathways

PB - Blackwell Publishing Inc.

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Jang SH, Lim JW, Kim HY. Mechanism of β-carotene-induced apoptosis of gastric cancer cells: Involvement of ataxia-telangiectasia-mutated. In Natural Compounds and Their Role in Apoptotic Cell Signaling Pathways. Blackwell Publishing Inc. 2009. p. 156-162. (Annals of the New York Academy of Sciences). https://doi.org/10.1111/j.1749-6632.2009.04711.x