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Application of AlDeSense to Stratify Ovarian Cancer Cells Based on Aldehyde Dehydrogenase 1A1 Activity
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ALDH1A2 Is a Candidate Tumor Suppressor Gene in Ovarian Cancer

Jung-A Choi1, Hyunja Kwon2, Hanbyoul Cho3

  • 1Department of Obstetrics and Gynecology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul 03722, Korea. jachoi@yuhs.ac.

Cancers
|October 17, 2019
PubMed

Insights

Aldehyde dehydrogenase 1 family member A2 (ALDH1A2) is downregulated in ovarian cancer, linked to poor prognosis. Its expression is epigenetically silenced by DNA methyltransferases, and restoring ALDH1A2 inhibits cancer cell growth.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Aldehyde dehydrogenase 1 family member A2 (ALDH1A2) is crucial for retinoic acid synthesis.
  • The specific function of ALDH1A2 in ovarian cancer pathogenesis is not well understood.
  • ALDH1A2 is among the most downregulated genes in ovarian cancer cells.

Purpose of the Study:

  • To investigate the role of ALDH1A2 in ovarian cancer.
  • To explore the epigenetic regulation of ALDH1A2 in ovarian cancer.
  • To determine the impact of ALDH1A2 expression on ovarian cancer progression.

Main Methods:

  • Complementary DNA microarray analysis to assess ALDH gene expression.
  • Analysis of ALDH1A2 expression in relation to patient survival data.
  • DNA methylation analysis and treatment with 5-aza-2'-deoxycytidine (DNA methylation inhibitor).
  • Silencing of DNA methyltransferase 1 (DNMT1) and DNMT3B.
  • Functional studies involving forced ALDH1A2 expression.

Main Results:

  • ALDH1A2 was significantly downregulated in ovarian cancer cells compared to normal cells.
  • Low ALDH1A2 expression correlated with unfavorable prognosis and reduced survival.
  • Hypermethylation of ALDH1A2 was prevalent in ovarian cancer, and its expression could be restored by demethylation agents.
  • Silencing DNMT1 or DNMT3B also restored ALDH1A2 expression.
  • Forced ALDH1A2 expression suppressed ovarian cancer cell proliferation and invasion.

Conclusions:

  • ALDH1A2 functions as a tumor suppressor in ovarian cancer.
  • ALDH1A2 expression is epigenetically regulated by DNA methyltransferases.
  • Restoring ALDH1A2 expression or its signaling pathways may offer novel therapeutic strategies for ovarian cancer.
Keywords:
ALDH1A2DNMTOVARIAN cancerinvasionmethylation

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