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Loss of TDP43 inhibits progression of triple-negative breast cancer in coordination with SRSF3

Hao Ke1,2, Limin Zhao1,2, Honglei Zhang1

  • 1State Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, 650223 Kunming, China.

Proceedings of the National Academy of Sciences of the United States of America
|March 28, 2018
PubMed

Insights

Triple-negative breast cancer (TNBC) progression is regulated by TAR DNA-binding protein 43 (TDP43). Targeting the TDP43/SRSF3 complex may offer new therapeutic strategies for TNBC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Aberrant alternative splicing is a recognized hallmark of cancer.
  • Triple-negative breast cancer (TNBC) exhibits a unique splicing profile.
  • The role of specific splicing regulators in TNBC remains to be fully elucidated.

Purpose of the Study:

  • To identify key splicing regulators involved in TNBC progression.
  • To investigate the functional role of TAR DNA-binding protein 43 (TDP43) in TNBC.
  • To explore the therapeutic potential of targeting splicing pathways in TNBC.

Main Methods:

  • Analysis of clinical TNBC data for TDP43 expression.
  • In vitro knockdown and overexpression studies of TDP43 in mammary epithelial cells.
  • Deep sequencing and functional assays to identify TDP43-regulated splicing events.
  • Investigation of the interaction between TDP43 and serine/arginine-rich splicing factor 3 (SRSF3).

Main Results:

  • TDP43 is highly expressed in TNBC and correlates with poor prognosis.
  • TDP43 knockdown inhibits TNBC cell proliferation and metastasis; overexpression promotes malignancy.
  • TDP43 collaborates with SRSF3 to regulate splicing events critical for TNBC progression.
  • Splicing regulation of PAR3 and NUMB exon 12 by the TDP43/SRSF3 complex mediates effects on proliferation and metastasis.

Conclusions:

  • TDP43 is a crucial splicing regulator in TNBC, driving tumor progression.
  • The TDP43/SRSF3 complex and its downstream targets, PAR3 and NUMB, represent potential therapeutic targets for TNBC.
  • Targeting this aberrant splicing axis offers a promising avenue for TNBC treatment strategies.
Keywords:
PAR3SRSF3TDP43alternative splicingbreast cancer

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