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Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
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Oligonucleotide-directed STAT3 alternative splicing switch drives anti-tumorigenic outcomes in MCF10 human breast

Vincent Tano1, David A Jans2, Marie A Bogoyevitch1

  • 1Department of Biochemistry and Molecular Biology, Medical Building, University of Melbourne, Parkville, VIC, 3010, Australia.

Biochemical and Biophysical Research Communications
|April 24, 2019
PubMed

Insights

Enhancing STAT3β spliceform expression in breast cancer cells reduces tumor growth, viability, and migration. This study explores the anti-tumorigenic effects of STAT3β, a shorter spliceform of Signal transducer and activator of transcription 3.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Signal transducer and activator of transcription 3 (STAT3) is a transcription factor with known oncogenic properties.
  • STAT3 exists as predominant STAT3α and shorter STAT3β spliceforms, with STAT3β showing potential tumor suppressive functions.
  • Modulating STAT3 alternative splicing to increase STAT3β levels offers a potential anti-cancer strategy.

Purpose of the Study:

  • To investigate the cellular mechanisms underlying the anti-tumorigenic effects of the STAT3β spliceform.
  • To evaluate the impact of increased STAT3β levels on breast cancer cell biology.
  • To assess the efficacy of spliceform-switching strategies in cancer therapy.

Main Methods:

  • Utilized Morpholino-based antisense oligonucleotides to modulate STAT3 spliceform expression in MCF10CA1h human breast cancer cells.
  • Employed nonsense-mediated decay (NMD) oligonucleotides for STAT3 knockdown and STAT3α-to-β expression switching (SWI) oligonucleotides to increase STAT3β levels.
  • Assessed the effects of STAT3 splicing modulation on cancer cell growth, viability, migration, and invasion.

Main Results:

  • SWI treatment significantly reduced MCF10CA1h cell growth, viability, and migration.
  • NMD treatment showed no significant impact on cancer cell phenotypes.
  • Neither NMD nor SWI oligonucleotides significantly inhibited cancer cell invasion through a semi-solid matrix.

Conclusions:

  • Redirecting STAT3 alternative splicing to favor STAT3β expression effectively suppresses breast cancer cell growth, viability, and migration.
  • STAT3β spliceform plays a crucial role in inhibiting key aspects of tumor progression.
  • Targeting STAT3 splicing represents a promising therapeutic avenue for breast cancer, particularly for reducing proliferation and metastasis.
Keywords:
Breast cancerInvasionMorpholino oligonucleotideProliferationSTAT3Viability

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