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Related Experiment Video

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In vitro Organoid Culture of Primary Mouse Colon Tumors
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Hypermethylation Of ADHFE1 Promotes The Proliferation Of Colorectal Cancer Cell Via Modulating Cell Cycle

Yu-Han Hu1, Shuai Ma1, Xiang-Nan Zhang2

  • 1Department of Pathology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, Henan 453000, People's Republic of China.

Oncotargets and Therapy
|October 22, 2019
PubMed
Summary
This summary is machine-generated.

Hypermethylation of the ADHFE1 gene is linked to colorectal cancer (CRC) progression. Restoring ADHFE1 expression inhibits CRC cell proliferation by affecting the cell cycle, offering a potential therapeutic target.

Keywords:
ADHFE1cell cyclecolorectal cancerhypermethylationproliferation

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Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Colorectal cancer (CRC) is a prevalent malignancy globally.
  • Epigenetic alterations are crucial in CRC development.
  • ADHFE1 gene hypermethylation is observed in CRC, but its functional role in proliferation is unknown.

Purpose of the Study:

  • To investigate the role and mechanism of ADHFE1 in colorectal cancer cell proliferation.
  • To determine the relationship between ADHFE1 expression, methylation, and clinicopathological features in CRC.

Main Methods:

  • Analyzed ADHFE1 expression in CRC tissues using IHC and qRT-PCR.
  • Assessed cell proliferation in vitro and in vivo.
  • Utilized GSEA, flow cytometry, Western blot, and BSP assay to explore mechanisms and methylation status.

Main Results:

  • ADHFE1 was found to be down-regulated and hypermethylated in CRC tissues.
  • Down-regulation correlated with poor differentiation and advanced TNM stage.
  • ADHFE1 overexpression inhibited CRC proliferation and induced G1-S cell cycle arrest, while knockdown promoted proliferation.

Conclusions:

  • ADHFE1 hypermethylation promotes CRC cell proliferation via cell cycle modulation.
  • Restoring ADHFE1 expression may offer a novel therapeutic strategy for colorectal cancer.