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Related Concept Videos

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Isolation and Functional Assessment of Human Breast Cancer Stem Cells from Cell and Tissue Samples
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HN1L Promotes Triple-Negative Breast Cancer Stem Cells through LEPR-STAT3 Pathway.

Yi Liu1, Dong Soon Choi1, Jianting Sheng2

  • 1Houston Methodist Cancer Center, Houston Methodist Hospital, 6445 Main Street, Floor 24, Houston, TX 77030, USA.

Stem Cell Reports
|December 19, 2017
PubMed
Summary

HEMATOLOGICAL AND NEUROLOGICAL EXPRESSED 1-LIKE (HN1L) is a key gene in breast cancer stem cells (BCSCs). Targeting HN1L may improve triple-negative breast cancer (TNBC) prognosis and therapy.

Keywords:
HN1LLEPRSTAT3TNBCcancer stem cells

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Breast cancer stem cells (BCSCs) drive tumor initiation and therapy resistance.
  • Triple-negative breast cancer (TNBC) lacks targeted therapies and has poor survival outcomes.
  • Identifying novel therapeutic targets in BCSCs is crucial for improving TNBC treatment.

Purpose of the Study:

  • To investigate the role of HEMATOLOGICAL AND NEUROLOGICAL EXPRESSED 1-LIKE (HN1L) in breast cancer, particularly in TNBC.
  • To determine if HN1L is a targetable gene in BCSCs.
  • To elucidate the molecular mechanisms by which HN1L influences BCSC function and TNBC progression.

Main Methods:

  • Gene expression analysis in breast cancer patient cohorts.
  • Functional studies involving HN1L gene silencing in TNBC cell lines and xenografts.
  • Investigation of HN1L's role in the LEPR-STAT3 signaling pathway.
  • Analysis of gene signatures associated with HN1L and patient survival.

Main Results:

  • HN1L is altered in 25% of breast cancers and associated with shorter survival in TNBC patients.
  • HN1L silencing reduced BCSC populations, inhibited tumor initiation, and overcame chemoresistance.
  • HN1L acts as a transcription regulator for genes in the LEPR-STAT3 pathway, including STAT3 and LEPTIN RECEPTOR.
  • HN1L-associated gene signatures correlate with shorter disease-free survival in TNBC.

Conclusions:

  • HN1L is a critical transcription regulator for BCSCs in TNBC, sustaining the LEPR-STAT3 pathway.
  • HN1L represents a potential prognostic marker and therapeutic target for TNBC.
  • Targeting HN1L could offer a novel strategy for BCSC-directed therapy in TNBC.