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  1. Home
  3. Znf8 Orchestrates With Smad3 To Promote Lung Metastasis By Recruiting Smyd3 In Breast Cancer.
  1. Home
  3. Znf8 Orchestrates With Smad3 To Promote Lung Metastasis By Recruiting Smyd3 In Breast Cancer.

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ZNF8 Orchestrates with Smad3 to Promote Lung Metastasis by Recruiting SMYD3 in Breast Cancer.

Wenwen Geng1,2, Junhua An1,2, Ke Dong1,2

  • 1Department of Breast Surgery, Qilu Hospital (Qingdao), Cheeloo College of Medicine, Shandong University, Qingdao, Shandong, 266000, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|September 3, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Researchers identified ZNF8 as a novel cofactor in the transforming growth factor-β (TGF-β) pathway that promotes breast cancer lung metastasis. Inhibiting SMYD3 effectively prevents this ZNF8-mediated metastasis, offering new therapeutic targets.

Keywords:
Smad3TGF‐β pathwayZNF8breast cancerlung metastasis

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Breast cancer metastasis, particularly to the lungs, is a primary cause of mortality.
  • The transforming growth factor-β (TGF-β) pathway, mediated by Smad3, is crucial for cancer metastasis.
  • Specific Smad3 cofactors driving lung metastasis remain largely unidentified.

Purpose of the Study:

  • To identify novel Smad3 cofactors involved in breast cancer lung metastasis.
  • To elucidate the mechanism by which these cofactors promote metastasis.
  • To explore potential therapeutic strategies targeting this pathway.

Main Methods:

  • Established the Smad3 interactome in breast cancer cells.
  • Identified and validated ZNF8 as a novel Smad3 cofactor.
  • Investigated the role of ZNF8 in TGF-β pathway-mediated metastasis and gene expression.
  • Assessed the effect of SMYD3 inhibition on ZNF8-mediated metastasis.

    • Main Results:

    • Identified ZNF8 as a novel Smad3 cofactor associated with poor breast cancer lung metastasis prognosis.
    • Demonstrated that ZNF8 facilitates TGF-β pathway-mediated lung metastasis.
    • Elucidated that ZNF8 enhances H3K4me3 modification and promotes metastasis signature gene expression by recruiting SMYD3.
    • Showed that SMYD3 inhibition (BCI121) effectively blocks ZNF8-mediated lung metastasis.

    Conclusions:

    • ZNF8 is a novel TGF-β/Smad3 cofactor that promotes breast cancer lung metastasis.
    • ZNF8 functions by enhancing H3K4me3 and recruiting SMYD3 to promote metastasis-associated gene expression.
    • Targeting SMYD3 presents a potential therapeutic strategy for managing breast cancer lung metastasis.