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Related Experiment Video

Updated: May 5, 2026

Methods to Discover Alternative Promoter Usage and Transcriptional Regulation of Murine Bcrp1
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Alternative Promoters Drive Transcriptomic Reprogramming and Prognostic Stratification in TNBC.

Simran Jit1,2, Kirti Jain1,2, Leepakshi Dhingra1

  • 1CSIR-Institute of Genomics and Integrative Biology (CSIR-IGIB), New Delhi, 110025, India.

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|October 31, 2025
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Summary

Alternative promoter usage impacts gene expression in Triple-Negative Breast Cancer (TNBC). This study reveals specific promoter switches and identifies novel biomarkers for predicting patient relapse-free survival.

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Area of Science:

  • Genomics
  • Cancer Biology
  • Epigenetics

Background:

  • Triple-Negative Breast Cancer (TNBC) is aggressive and heterogeneous, with gene expression poorly understood at the pre-transcriptional level.
  • Short-read RNA sequencing has limitations in resolving transcript diversity, hindering the study of alternative promoter usage.
  • Alternative promoter usage is a critical regulatory mechanism in cancer, yet remains underexplored in TNBC.

Purpose of the Study:

  • To investigate promoter-level quantification for inferring active promoter usage in TNBC.
  • To identify TNBC-specific and subtype-enriched Active Alternative Promoters (AAPs).
  • To explore the prognostic value of alternative promoter activity in TNBC patient outcomes.

Main Methods:

  • Utilized RNA-sequencing data from 360 TNBC tumors and 88 normal tissues for promoter-level quantification.
  • Integrated data with H3K4me3 and H3K27ac ChIP-seq to analyze epigenetic modifications.
  • Developed a prognostic model incorporating promoter activities and clinical variables.

Main Results:

  • Identified TNBC-specific AAPs and a key promoter switch in the HDAC9 gene, epigenetically regulated.
  • Discovered subtype-specific alternative promoter activities (e.g., SEC31A, AKAP9) not evident at the gene expression level.
  • Alternative promoters of HUWE1 and FTX independently predicted relapse-free survival (RFS) in TNBC.

Conclusions:

  • Promoter switching in genes like HDAC9 is a tumor-specific regulatory mechanism in TNBC.
  • Alternative promoter analysis provides insights into TNBC heterogeneity and regulation.
  • Promoter activity represents a promising biomarker for improving TNBC risk stratification and predicting patient prognosis.