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Related Experiment Video

Updated: Apr 8, 2026

3-D Cell Culture System for Studying Invasion and Evaluating Therapeutics in Bladder Cancer
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UCHL3 Promotes Triple-Negative Breast Cancer Metastatic Potential Through Enhancing Cell Migration and Invasion.

Qi Xu1,2, Wenli Yang1, Chengxia Li1

  • 1Institute for Cancer Medicine, School of Basic Medical Sciences, Southwest Medical University, Luzhou, 646000, China.

Applied Biochemistry and Biotechnology
|April 7, 2026
PubMed
Summary

Ubiquitin carboxyl-terminal hydrolase L3 (UCHL3) promotes triple-negative breast cancer (TNBC) progression by increasing cell proliferation and driving metastasis. Targeting UCHL3 may offer a new therapeutic strategy for TNBC treatment.

Keywords:
De-ubiquitinationEMTMigrationTNBCUCHL3

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Ubiquitin carboxyl-terminal hydrolase L3 (UCHL3) is a deubiquitinating enzyme implicated in DNA repair.
  • Its role in triple-negative breast cancer (TNBC) cell migration and invasion is not well understood.
  • Understanding UCHL3's function in TNBC is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of UCHL3 in regulating cell migration, invasion, and proliferation in TNBC.
  • To explore the underlying molecular mechanisms of UCHL3 action in TNBC.
  • To evaluate UCHL3 as a potential therapeutic target for TNBC.

Main Methods:

  • Analysis of TCGA data for UCHL3 expression across breast cancer subtypes.
  • qRT-PCR and Western blot to assess UCHL3 and EMT marker expression in TNBC cells.
  • In vitro functional assays (MTT, EdU, wound healing, Transwell) and RNA sequencing.
  • In vivo mouse model to assess the effect of UCHL3 overexpression on TNBC metastasis.

Main Results:

  • UCHL3 is significantly overexpressed in TNBC and correlates with poor patient prognosis.
  • UCHL3 enhances TNBC cell proliferation, migration, and invasion by modulating EMT markers.
  • Knockdown of UCHL3 attenuates invasion- and migration-related signaling pathways.
  • Pharmacological inhibition of UCHL3 suppresses TNBC cell migration and invasion in vitro and in vivo.

Conclusions:

  • UCHL3 is upregulated in TNBC and drives tumor progression through enhanced proliferation and EMT-mediated invasion.
  • UCHL3 plays a critical role in promoting TNBC cell migration and metastasis.
  • UCHL3 represents a promising therapeutic target for TNBC treatment.