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 S. Kim; Sun Hwa Park

doi:10.1186/1471-2407-14-377

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 S. Kim, Sun Hwa Park

Research output: Contribution to journal › Article › peer-review

26 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 language	English
Article number	377
Journal	BMC Cancer
Volume	14
Issue number	1
DOIs	https://doi.org/10.1186/1471-2407-14-377
Publication status	Published - 2014 May 28

Bibliographical note

Funding Information:
This study was supported by a Korea University Grant (K1132261) and the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (grant number: 2010–0024117).

Keywords

ADHFE1
Alcohol
Colorectal cancer
Hypermethylation
Quantitative methylation-specific polymerase chain reaction

ASJC Scopus subject areas

Genetics
Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1186/1471-2407-14-377

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@article{6970db089f16494d94860de9a494c54a,

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.",

keywords = "ADHFE1, Alcohol, Colorectal cancer, Hypermethylation, Quantitative methylation-specific polymerase chain reaction",

author = "Moon, {Ji W.} and Lee, {Soo K.} and Lee, {Yong W.} and Lee, {Jung O.} and Nami Kim and Lee, {Hye J.} and Seo, {Jung S.} and Jin Kim and Kim, {Hyeon S.} and Park, {Sun Hwa}",

note = "Funding Information: This study was supported by a Korea University Grant (K1132261) and the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (grant number: 2010–0024117).",

year = "2014",

month = may,

day = "28",

doi = "10.1186/1471-2407-14-377",

language = "English",

volume = "14",

journal = "BMC Cancer",

issn = "1471-2407",

publisher = "BioMed Central",

number = "1",

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TY - JOUR

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 S.

AU - Park, Sun Hwa

N1 - Funding Information: This study was supported by a Korea University Grant (K1132261) and the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (grant number: 2010–0024117).

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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U2 - 10.1186/1471-2407-14-377

DO - 10.1186/1471-2407-14-377

M3 - Article

C2 - 24886599

AN - SCOPUS:84902364121

SN - 1471-2407

VL - 14

JO - BMC Cancer

JF - BMC Cancer

IS - 1

M1 - 377

ER -

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

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

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