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ATXN7L3 positively regulates SMAD7 transcription in hepatocellular carcinoma with growth inhibitory function

Ning Sun1, Xinping Zhong2, Shengli Wang1

  • 1Department of Cell Biology, Key laboratory of Cell Biology, Ministry of Public Health, and Key laboratory of Medical Cell Biology, Ministry of Education, School of Life Sciences, China Medical University, Shenyang City, Liaoning Province 110122, China.

Ebiomedicine
|November 13, 2020
PubMed
Abstract

Insights

ATXN7L3 acts as a tumor suppressor in hepatocellular carcinoma (HCC) by regulating SMAD7 transcription and inhibiting tumor growth. Lower ATXN7L3 expression correlates with poor HCC patient outcomes, suggesting its potential as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • Hepatocellular carcinoma (HCC) presents a significant global health challenge with limited effective pharmacological treatments.
  • The specific role of ATXN7L3 in the progression of HCC remains largely unexplored.

Purpose of the Study:

  • To elucidate the function of ATXN7L3 in hepatocellular carcinoma (HCC) progression.
  • To investigate the molecular mechanisms underlying ATXN7L3's role in HCC.

Main Methods:

  • Gene expression analysis using RNA sequencing, qRT-PCR, and Western blot.
  • Chromatin immunoprecipitation (ChIP) to determine molecular mechanisms.
  • In vitro and in vivo assays including colony formation, cell growth curves, and xenograft tumor experiments.

Main Results:

  • ATXN7L3 functions as a coactivator for ERα, enhancing SMAD7 transcription via recruitment to promoter regions and regulating histone H2B ubiquitination.
  • ATXN7L3 expression is significantly lower in HCC tissues and correlates with poorer clinical outcomes.
  • ATXN7L3 demonstrates tumor-suppressive activity, inhibiting HCC cell growth both in vitro and in vivo.

Conclusions:

  • ATXN7L3 is identified as a novel regulator of SMAD7 transcription and a suppressor of tumor growth in HCC.
  • This study highlights a previously unrecognized role for ATXN7L3 in HCC pathogenesis, offering potential therapeutic insights.
Keywords:
ATXN7L3Co-regulatorDeubiquitination modificationEstrogen receptor αHepatocellular carcinoma

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