Related Experiment Video

Updated: Jun 24, 2025

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter
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YY1 mediated DCUN1D5 transcriptional activation promotes triple-negative breast cancer progression by targeting

Yuxiang Lin1,2,3, Yan Li1,2,3, Xiaobin Chen1,2,3

  • 1Department of Breast Surgery, Fujian Medical University Union Hospital, No.29, Xin Quan Road, Gulou District, Fuzhou, 350001, Fujian Province, China.

Biology Direct
|June 3, 2024
PubMed

Insights

Defective in cullin neddylation 1 domain containing 5 (DCUN1D5) promotes triple-negative breast cancer (TNBC) progression. Targeting DCUN1D5 may offer new therapeutic strategies for aggressive TNBC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Triple-negative breast cancer (TNBC) exhibits aggressive behavior and high metastasis rates.
  • Current TNBC treatment options are limited due to a lack of specific drug targets, leading to resistance and poor outcomes.
  • Novel molecular biomarkers and therapeutic targets are crucial for improving TNBC patient prognosis.

Purpose of the Study:

  • To investigate the role and mechanism of Defective in cullin neddylation 1 domain containing 5 (DCUN1D5) in triple-negative breast cancer (TNBC) progression.
  • To identify DCUN1D5 as a potential prognostic biomarker and therapeutic target for TNBC.

Main Methods:

  • Analysis of The Cancer Genome Atlas (TCGA) dataset and immunohistochemical (IHC) staining of surgical specimens.
  • In vitro and in vivo experiments to confirm the oncogenic role of DCUN1D5.
  • Investigation of the regulatory pathway involving Yin Yang 1 (YY1), DCUN1D5, and the FN1/PI3K/AKT pathway.

Main Results:

  • DCUN1D5 was significantly upregulated in TNBC tissues and negatively correlated with patient prognosis.
  • DCUN1D5 overexpression was confirmed to promote TNBC proliferation and invasion.
  • DCUN1D5 acts as a transcriptional target of YY1, promoting TNBC progression via the FN1/PI3K/AKT pathway.

Conclusions:

  • YY1-enhanced DCUN1D5 expression drives TNBC progression through the FN1/PI3K/AKT signaling pathway.
  • DCUN1D5 represents a promising prognostic biomarker and a potential therapeutic target for TNBC treatment.
  • Further research into the YY1-DCUN1D5 axis could lead to novel therapeutic strategies for TNBC.
Keywords:
DCUN1D5FN1ProgressionTriple-negative breast cancerYY1

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