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Function of UDP-glucuronosyltransferase 2B17 (UGT2B17) is involved in endometrial cancer

Hiroshi Hirata1, Yuji Hinoda, Mohd S Zaman

  • 1Department of Urology, Veterans Affairs Medical Center and University of California at San Francisco, 4150 Clement Street, San Francisco, CA 94121, USA.

Carcinogenesis
|June 18, 2010
PubMed

Insights

Uridine 5'-diphospho-glucuronosyltransferase 17 (UGT2B17) and myeloid cell leukemia-1 (Mcl-1) are upregulated in endometrial cancer. Depleting UGT2B17 inhibits cancer cell growth and promotes apoptosis by downregulating Mcl-1.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Endometrial cancer (EC) is a steroid hormone-dependent malignancy.
  • Uridine 5'-diphospho-glucuronosyltransferase (UGT) enzymes detoxify hormones and carcinogens.
  • The specific role of UGT2B17 in EC remains largely uncharacterized.

Purpose of the Study:

  • To investigate the function of UGT2B17 in endometrial cancer.
  • To determine the relationship between UGT2B17 and myeloid cell leukemia-1 (Mcl-1) expression in EC.
  • To elucidate the molecular mechanisms underlying UGT2B17's role in EC progression.

Main Methods:

  • Analysis of UGT2B17 and Mcl-1 mRNA expression in EC tissues versus normal tissues.
  • Functional assays (cell growth, invasion, apoptosis, cell cycle) in EC cell lines with UGT2B17 knockdown.
  • Microarray analysis to identify UGT2B17 target genes.

Main Results:

  • UGT2B17 and Mcl-1 mRNA expression were significantly elevated in EC tissues.
  • Knockdown of UGT2B17 in EC cells led to reduced cell viability and increased apoptosis.
  • Microarray analysis revealed Mcl-1 as a direct target gene downregulated by UGT2B17 depletion, leading to Puma protein upregulation.

Conclusions:

  • UGT2B17 and Mcl-1 are upregulated in endometrial cancer.
  • UGT2B17 depletion inhibits EC cell proliferation and induces apoptosis, mediated by Mcl-1 downregulation.
  • UGT2B17 represents a potential therapeutic target for endometrial cancer.

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