High-level expression of ARID1A predicts a favourable outcome in triple-negative breast cancer patients receiving paclitaxel-based chemotherapy

Yuan Feng Lin, Ing Jy Tseng, Chih Jung Kuo, Hui Yu Lin, I. Jen Chiu, Hui Wen Chiu

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Paclitaxel-based chemotherapy is a common strategy to treat patients with triple-negative breast cancer (TNBC). As paclitaxel resistance is still a clinical issue in treating TNBCs, identifying molecular markers for predicting pathologic responses to paclitaxel treatment is thus urgently needed. Here, we report that an AT-rich interaction domain 1A (ARID1A) transcript is up-regulated in paclitaxel-sensitive TNBC cells but down-regulated in paclitaxel-resistant cells upon paclitaxel treatment. Moreover, ARID1A expression was negatively correlated with the IC50 concentration of paclitaxel in the tested TNBC cell lines. Kaplan-Meier analyses revealed that ARID1A down-regulation was related to a poorer response to paclitaxel-based chemotherapy in patients with TNBCs as measured by the recurrence-free survival probability. The pharmaceutical inhibition with p38MAPK-specific inhibitor SCIO-469 revealed that p38MAPK-related signalling axis regulates ARID1A expression and thereby modulates paclitaxel sensitivity in TNBC cells. These findings suggest that ARID1A could be used as a prognostic factor to estimate the pathological complete response for TNBC patients who decide to receive paclitaxel-based chemotherapy.

Original languageEnglish
Pages (from-to)2458-2468
Number of pages11
JournalJournal of Cellular and Molecular Medicine
Volume22
Issue number4
DOIs
Publication statusPublished - Apr 1 2018

Keywords

  • ARID1A
  • Chemotherapy
  • P38MAPK
  • Paclitaxel
  • Triple-negative breast cancer

ASJC Scopus subject areas

  • Molecular Medicine
  • Cell Biology

Fingerprint Dive into the research topics of 'High-level expression of ARID1A predicts a favourable outcome in triple-negative breast cancer patients receiving paclitaxel-based chemotherapy'. Together they form a unique fingerprint.

  • Cite this