Alcohol induces cell proliferation via hypermethylation of ADHFE1 in colorectal cancer cells

Ji W. Moon, Soo K. Lee, Yong W. Lee, Jung O. Lee, Nami Kim, Hye J. Lee, Jung S. Seo, Jin Kim, Hyeon Soo Kim, Sun-Hwa Park

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Background: The hypermethylation of Alcohol dehydrogenase iron containing 1 (ADHFE1) was recently reported to be associated with colorectal cancer (CRC) differentiation. However, the effect of alcohol on ADHFE1 hypermethylation in CRC is still unclear.Methods: The methylation status and expression levels of ADHFE1 were investigated in primary tumor tissues and adjacent normal tissues of 73 patients with CRC, one normal colon cell line, and 4 CRC cell lines (HT-29, SW480, DLD-1, and LoVo) by quantitative methylation-specific polymerase chain reaction (QMSP) and real-time reverse transcription polymerase chain reaction (real time PCR), respectively. The effect of alcohol on the methylation status of ADHFE1 was analyzed in HT-29, SW480, DLD-1, and CCD18Co cells using QMSP, real-time PCR, immunoblot, and cell proliferation assay.Results: ADHFE1 was hypermethylated in 69 of 73 CRC tissues (95%) compared to adjacent normal tissues (p < 0.05). The mRNA expression of ADHFE1 was significantly reduced in CRC compared to adjacent normal tissues (p < 0.05) and its expression was decreased in the alcohol consumption group (p < 0.05). ADHFE1 was hypermethylated and its expression was decreased in 4 CRC cell lines compared with normal colon cell line. Alcohol induced hypermethylation of ADHFE1, decreased its expression, and stimulated cell proliferation of HT-29, SW480, and DLD-1cells.Conclusion: These results demonstrate that the promoter hypermethylation of ADHFE1 is frequently present in CRC and alcohol induces methylation-mediated down expression of ADHFE1 and proliferation of CRC cells.

Original languageEnglish
Article number377
JournalBMC Cancer
Volume14
Issue number1
DOIs
Publication statusPublished - 2014 May 28

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Colorectal Neoplasms
Alcohols
Cell Proliferation
Methylation
Cell Line
Real-Time Polymerase Chain Reaction
Colon
Polymerase Chain Reaction
Alcohol Dehydrogenase
Alcohol Drinking
Reverse Transcription
Iron
Messenger RNA
Neoplasms

ASJC Scopus subject areas

  • Oncology
  • Cancer Research
  • Genetics

Cite this

Alcohol induces cell proliferation via hypermethylation of ADHFE1 in colorectal cancer cells. / Moon, Ji W.; Lee, Soo K.; Lee, Yong W.; Lee, Jung O.; Kim, Nami; Lee, Hye J.; Seo, Jung S.; Kim, Jin; Kim, Hyeon Soo; Park, Sun-Hwa.

In: BMC Cancer, Vol. 14, No. 1, 377, 28.05.2014.

Research output: Contribution to journalArticle

Moon, Ji W. ; Lee, Soo K. ; Lee, Yong W. ; Lee, Jung O. ; Kim, Nami ; Lee, Hye J. ; Seo, Jung S. ; Kim, Jin ; Kim, Hyeon Soo ; Park, Sun-Hwa. / Alcohol induces cell proliferation via hypermethylation of ADHFE1 in colorectal cancer cells. In: BMC Cancer. 2014 ; Vol. 14, No. 1.
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title = "Alcohol induces cell proliferation via hypermethylation of ADHFE1 in colorectal cancer cells",
abstract = "Background: The hypermethylation of Alcohol dehydrogenase iron containing 1 (ADHFE1) was recently reported to be associated with colorectal cancer (CRC) differentiation. However, the effect of alcohol on ADHFE1 hypermethylation in CRC is still unclear.Methods: The methylation status and expression levels of ADHFE1 were investigated in primary tumor tissues and adjacent normal tissues of 73 patients with CRC, one normal colon cell line, and 4 CRC cell lines (HT-29, SW480, DLD-1, and LoVo) by quantitative methylation-specific polymerase chain reaction (QMSP) and real-time reverse transcription polymerase chain reaction (real time PCR), respectively. The effect of alcohol on the methylation status of ADHFE1 was analyzed in HT-29, SW480, DLD-1, and CCD18Co cells using QMSP, real-time PCR, immunoblot, and cell proliferation assay.Results: ADHFE1 was hypermethylated in 69 of 73 CRC tissues (95{\%}) compared to adjacent normal tissues (p < 0.05). The mRNA expression of ADHFE1 was significantly reduced in CRC compared to adjacent normal tissues (p < 0.05) and its expression was decreased in the alcohol consumption group (p < 0.05). ADHFE1 was hypermethylated and its expression was decreased in 4 CRC cell lines compared with normal colon cell line. Alcohol induced hypermethylation of ADHFE1, decreased its expression, and stimulated cell proliferation of HT-29, SW480, and DLD-1cells.Conclusion: These results demonstrate that the promoter hypermethylation of ADHFE1 is frequently present in CRC and alcohol induces methylation-mediated down expression of ADHFE1 and proliferation of CRC cells.",
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T1 - Alcohol induces cell proliferation via hypermethylation of ADHFE1 in colorectal cancer cells

AU - Moon, Ji W.

AU - Lee, Soo K.

AU - Lee, Yong W.

AU - Lee, Jung O.

AU - Kim, Nami

AU - Lee, Hye J.

AU - Seo, Jung S.

AU - Kim, Jin

AU - Kim, Hyeon Soo

AU - Park, Sun-Hwa

PY - 2014/5/28

Y1 - 2014/5/28

N2 - Background: The hypermethylation of Alcohol dehydrogenase iron containing 1 (ADHFE1) was recently reported to be associated with colorectal cancer (CRC) differentiation. However, the effect of alcohol on ADHFE1 hypermethylation in CRC is still unclear.Methods: The methylation status and expression levels of ADHFE1 were investigated in primary tumor tissues and adjacent normal tissues of 73 patients with CRC, one normal colon cell line, and 4 CRC cell lines (HT-29, SW480, DLD-1, and LoVo) by quantitative methylation-specific polymerase chain reaction (QMSP) and real-time reverse transcription polymerase chain reaction (real time PCR), respectively. The effect of alcohol on the methylation status of ADHFE1 was analyzed in HT-29, SW480, DLD-1, and CCD18Co cells using QMSP, real-time PCR, immunoblot, and cell proliferation assay.Results: ADHFE1 was hypermethylated in 69 of 73 CRC tissues (95%) compared to adjacent normal tissues (p < 0.05). The mRNA expression of ADHFE1 was significantly reduced in CRC compared to adjacent normal tissues (p < 0.05) and its expression was decreased in the alcohol consumption group (p < 0.05). ADHFE1 was hypermethylated and its expression was decreased in 4 CRC cell lines compared with normal colon cell line. Alcohol induced hypermethylation of ADHFE1, decreased its expression, and stimulated cell proliferation of HT-29, SW480, and DLD-1cells.Conclusion: These results demonstrate that the promoter hypermethylation of ADHFE1 is frequently present in CRC and alcohol induces methylation-mediated down expression of ADHFE1 and proliferation of CRC cells.

AB - Background: The hypermethylation of Alcohol dehydrogenase iron containing 1 (ADHFE1) was recently reported to be associated with colorectal cancer (CRC) differentiation. However, the effect of alcohol on ADHFE1 hypermethylation in CRC is still unclear.Methods: The methylation status and expression levels of ADHFE1 were investigated in primary tumor tissues and adjacent normal tissues of 73 patients with CRC, one normal colon cell line, and 4 CRC cell lines (HT-29, SW480, DLD-1, and LoVo) by quantitative methylation-specific polymerase chain reaction (QMSP) and real-time reverse transcription polymerase chain reaction (real time PCR), respectively. The effect of alcohol on the methylation status of ADHFE1 was analyzed in HT-29, SW480, DLD-1, and CCD18Co cells using QMSP, real-time PCR, immunoblot, and cell proliferation assay.Results: ADHFE1 was hypermethylated in 69 of 73 CRC tissues (95%) compared to adjacent normal tissues (p < 0.05). The mRNA expression of ADHFE1 was significantly reduced in CRC compared to adjacent normal tissues (p < 0.05) and its expression was decreased in the alcohol consumption group (p < 0.05). ADHFE1 was hypermethylated and its expression was decreased in 4 CRC cell lines compared with normal colon cell line. Alcohol induced hypermethylation of ADHFE1, decreased its expression, and stimulated cell proliferation of HT-29, SW480, and DLD-1cells.Conclusion: These results demonstrate that the promoter hypermethylation of ADHFE1 is frequently present in CRC and alcohol induces methylation-mediated down expression of ADHFE1 and proliferation of CRC cells.

KW - ADHFE1

KW - Alcohol

KW - Colorectal cancer

KW - Hypermethylation

KW - Quantitative methylation-specific polymerase chain reaction

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