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The deubiquitinating enzyme ATXN3 promotes the progression of anaplastic thyroid carcinoma by stabilizing EIF5A2

Shimin Zhuang1, Jing Xie2, Jing Zhen2

  • 1Department of Otolaryngology-Head & Neck Surgery, The Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.

Molecular and Cellular Endocrinology
|August 24, 2021
PubMed

Insights

Ataxin-3 (ATXN3) is overexpressed in anaplastic thyroid carcinoma (ATC), promoting cancer cell proliferation and metastasis. ATXN3 targets EIF5A2, offering a potential therapeutic target for ATC progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Ataxin-3 (ATXN3) is a deubiquitinating enzyme involved in various cancers.
  • The role of ATXN3 in anaplastic thyroid carcinoma (ATC) pathogenesis is currently unknown.

Purpose of the Study:

  • To investigate the functional role of ATXN3 in anaplastic thyroid carcinoma (ATC).
  • To elucidate the underlying mechanisms by which ATXN3 influences ATC progression.

Main Methods:

  • Quantitative analysis of ATXN3 expression in ATC versus paracancerous tissues.
  • In vitro gain- and loss-of-function assays to assess ATXN3's impact on ATC cell behavior.
  • Correlation analysis between ATXN3 and eukaryotic translation initiation factor 5A2 (EIF5A2) protein levels.
  • Mechanistic studies involving ATXN3 binding, ubiquitination, and degradation of EIF5A2.

Main Results:

  • ATXN3 is significantly overexpressed in ATC tissues compared to adjacent normal tissues.
  • Overexpression of ATXN3 enhances proliferation and metastasis of ATC cells.
  • ATXN3 positively correlates with EIF5A2 levels in ATC.
  • ATXN3 promotes ATC proliferation and metastasis by stabilizing EIF5A2 via direct binding and reduced ubiquitination/degradation.

Conclusions:

  • ATXN3 plays a crucial role in the carcinogenesis of ATC.
  • The ATXN3/EIF5A2 axis represents a novel mechanism driving ATC progression.
  • ATXN3 emerges as a potential therapeutic target for managing anaplastic thyroid carcinoma.
Keywords:
ATCATXN3DeubiquitinationEIF5A2MigrationProliferation

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