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Differential Expression and Pathway Analysis in Drug-Resistant Triple-Negative Breast Cancer Cell Lines Using RNASeq

Safa Shaheen1, Febin Fawaz2, Shaheen Shah3

  • 1Genomics Central, Thrissur 680125, India. safashaheenshah@gmail.com.

International Journal of Molecular Sciences
|June 21, 2018
PubMed

Insights

Triple-negative breast cancer (TNBC) drug resistance mechanisms were investigated using RNA sequencing. The cytokine-cytokine receptor interaction pathway emerged as a critical factor in TNBC treatment unresponsiveness.

Area of Science:

  • Oncology
  • Genomics
  • Molecular Biology

Background:

  • Triple-negative breast cancer (TNBC) presents treatment challenges due to receptor absence (estrogen receptor, progesterone receptor, HER2) and molecular variability.
  • Drug resistance significantly contributes to treatment failures in TNBC patients.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying drug resistance in TNBC.
  • To identify key biological pathways involved in TNBC drug resistance using RNA sequencing data.

Main Methods:

  • RNA sequencing (RNA-Seq) analysis of two TNBC cell lines (SUM159, MDA-MB-231) resistant to JQ1 and Dexamethasone.
  • Differential gene expression analysis using edgeR to identify significant Differentially Expressed Genes (DEGs).
  • Pathway analysis including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) using iPathway analysis for validation.

Main Results:

  • Identified significant similarities and differences in gene expression profiles between TNBC cell lines, highlighting molecular heterogeneity.
  • The cytokine-cytokine receptor interaction pathway was identified as a key pathway implicated in TNBC drug resistance.

Conclusions:

  • Understanding TNBC molecular heterogeneity is crucial for developing strategies to overcome drug resistance.
  • Targeting the cytokine-cytokine receptor interaction pathway may offer a therapeutic approach to improve treatment outcomes in TNBC.
Keywords:
RNASeqTriple-negative breast cancerbasal bcytokine-cytokine receptor interactiondrug resistance

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