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Effects of Sepantronium Bromide (YM-155) on the Whole Transcriptome of MDA-MB-231 Cells: Highlight on Impaired

Elizabeth A Mazzio1, Charles A Lewis1, Rashid Elhag1

  • 1College of Pharmacy & Pharmaceutical Sciences, Florida A&M University, Tallahassee, FL, U.S.A.

Cancer Genomics & Proteomics
|July 7, 2018
PubMed

Insights

Sepantronium bromide (YM-155) reduces survivin mRNA and protein, but its primary impact is disrupting DNA repair systems. This drug significantly alters gene expression, affecting pathways crucial for tumor suppression and DNA damage response.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genomics

Background:

  • Sepantronium bromide (YM-155) is investigated for its potential to induce apoptosis and mitotic arrest in cancer cells.
  • The drug's mechanism is hypothesized to involve the reduction of survivin (BIRC5) mRNA levels.

Purpose of the Study:

  • To investigate the effects of YM-155 on survivin mRNA and protein expression in MDA-MB-231 cells.
  • To evaluate the whole transcriptomic and long intergenic non-coding RNA changes induced by YM-155 at sub-lethal and lethal concentrations.

Main Methods:

  • Treatment of MDA-MB-231 cells with YM-155 at 83 ng/mL (sub-lethal) and 14.6 ng/mL (LC50).
  • Monitoring of survivin mRNA and protein levels.
  • Whole transcriptome (WT) and long intergenic non-coding RNA profiling at 8 and 20 hours post-treatment.

Main Results:

  • A significant decrease in survivin mRNA and protein was observed at 20 hours (LC50), correlating with cell death.
  • Over 2000 differentially expressed transcripts were identified, indicating broad transcriptomic alterations.
  • YM-155 upregulated genes involved in circadian rhythm, tumor suppression, and NF-kappa B signaling.
  • Downregulated genes included those related to DNA damage repair, micro-RNAs, and notably, the ATM/Fanconi anemia pathway.

Conclusions:

  • The observed cell death and survivin reduction by YM-155 are closely linked.
  • YM-155 causes extensive transcriptomic changes beyond survivin modulation.
  • The drug's primary mechanism appears to be the disruption of replicative DNA repair systems, including the ATM and Fanconi anemia pathways.
Keywords:
Fanconi anemiaSepantronium bromideYM-155transcriptome

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