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Overexpression of SLAP2 inhibits triple-negative breast cancer progression by promoting macrophage M1-type polarization

  • 0Department of Breast Cancer Center, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, National Key Clinical Specialty, Hubei Provincial Clinical Research Center for Breast Cancer, Wuhan Clinical Research Center for Breast Cancer, No.116 Zhuo Daoquan South Road, Wuhan, 430079, Hubei, China.
Scientific Reports +

|

October 30, 2024

|

October 30, 2024

View abstract on PubMed

Summary

This summary is machine-generated.

Overexpression of Src-like adaptor protein 2 (SLAP2) inhibits triple-negative breast cancer (TNBC) progression by promoting M1 macrophage polarization. This study reveals SLAP2 as a potential therapeutic target for TNBC by modulating the tumor immune microenvironment.

Area Of Science

  • Oncology
  • Immunology
  • Molecular Biology

Background

  • Triple-negative breast cancer (TNBC) is an aggressive subtype with poor prognosis.
  • Src-like adaptor protein 2 (SLAP2) is implicated in regulating signaling pathways relevant to cancer.
  • Understanding SLAP2's role in TNBC is crucial for developing targeted therapies.

Purpose Of The Study

  • To investigate the effects of SLAP2 overexpression on TNBC progression.
  • To elucidate the underlying mechanisms, focusing on macrophage polarization.
  • To assess SLAP2's impact on tumor growth, invasion, and apoptosis.

Main Methods

  • Constructed SLAP2 overexpressing lentivirus in MDA-MB-231 (TNBC) and 4T1 (mouse TNBC) cell lines.
  • Utilized mRNA high-throughput sequencing (RNA-Seq) and bioinformatics for gene expression analysis.
  • Assessed tumor growth, apoptosis, and macrophage polarization in vivo (nude mice) and in vitro (transwell co-culture).

Main Results

  • SLAP2 overexpression altered gene expression, primarily related to immune response.
  • In vivo, SLAP2 overexpression inhibited tumor growth, reduced proliferation marker Ki67, and increased apoptosis.
  • SLAP2 promoted M1 macrophage polarization and inhibited M2 polarization, impacting TNBC cell behavior.

Conclusions

  • SLAP2 overexpression inhibits TNBC progression by promoting M1 macrophage polarization.
  • SLAP2 influences tumor immunity and malignant behavior through macrophage modulation.
  • SLAP2 represents a potential therapeutic target for triple-negative breast cancer.

Keywords:

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