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Modulation of alternative splicing induced by paclitaxel in human lung cancer

Ziran Zhu1, Dan Chen2, Wenjing Zhang1

  • 1Institute of Cancer Stem Cell & Radiotherapy Oncology Department of the Second Affiliated Hospital, Dalian Medical University, Dalian, 116044, China.

Cell Death & Disease
|May 1, 2018
PubMed

Insights

Paclitaxel, a chemotherapy drug, inhibits non-small-cell lung cancer progression by altering RNA splicing. It promotes the production of short ECT2 splicing isoforms, suppressing cancer cell proliferation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Paclitaxel is a primary chemotherapy for advanced non-small-cell lung carcinoma.
  • The role of paclitaxel in regulating RNA alternative splicing for cancer suppression is not well understood.

Purpose of the Study:

  • To investigate the effects of paclitaxel on cancer progression via RNA alternative splicing.
  • To elucidate the molecular mechanisms underlying paclitaxel's anti-cancer activity.

Main Methods:

  • Assessing paclitaxel's impact on cell proliferation, cell cycle arrest, and apoptosis.
  • Analyzing transcriptional changes in response to paclitaxel.
  • Identifying and characterizing paclitaxel-modulated RNA alternative splicing events.

Main Results:

  • Paclitaxel inhibits cell proliferation, induces cell cycle arrest, and promotes apoptosis.
  • Paclitaxel alters gene expression networks involved in DNA replication, repair, mitosis, and chromatin silencing.
  • Paclitaxel specifically modulates splicing of ECT2, favoring the production of short isoforms (ECT2-S), which inhibits cancer cell proliferation.

Conclusions:

  • Paclitaxel's anti-cancer effects are partly mediated by the regulation of RNA alternative splicing.
  • Modulating RNA splicing, particularly of ECT2, offers a potential novel therapeutic strategy for paclitaxel in cancer treatment.

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