High‐level expression of ARID1A predicts a favourable outcome in triple‐negative breast cancer patients receiving paclitaxel‐based chemotherapy
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. Her...
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Published in | Journal of cellular and molecular medicine Vol. 22; no. 4; pp. 2458 - 2468 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
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England
John Wiley & Sons, Inc
01.04.2018
John Wiley and Sons Inc |
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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. |
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AbstractList | 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.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. 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. 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 IC 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. 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 TNBC s, identifying molecular markers for predicting pathologic responses to paclitaxel treatment is thus urgently needed. Here, we report that an AT ‐rich interaction domain 1A ( ARID 1A ) transcript is up‐regulated in paclitaxel‐sensitive TNBC cells but down‐regulated in paclitaxel‐resistant cells upon paclitaxel treatment. Moreover, ARID 1A expression was negatively correlated with the IC 50 concentration of paclitaxel in the tested TNBC cell lines. Kaplan‐Meier analyses revealed that ARID 1A down‐regulation was related to a poorer response to paclitaxel‐based chemotherapy in patients with TNBC s as measured by the recurrence‐free survival probability. The pharmaceutical inhibition with p38 MAPK ‐specific inhibitor SCIO ‐469 revealed that p38 MAPK ‐related signalling axis regulates ARID 1A expression and thereby modulates paclitaxel sensitivity in TNBC cells. These findings suggest that ARID 1A could be used as a prognostic factor to estimate the pathological complete response for TNBC patients who decide to receive paclitaxel‐based chemotherapy. |
Author | Lin, Hui‐Yu Kuo, Chih‐Jung Lin, Yuan‐Feng Chiu, I‐Jen Chiu, Hui‐Wen Tseng, Ing‐Jy |
AuthorAffiliation | 5 Division of Nephrology Department of Internal Medicine Shuang Ho Hospital Taipei Medical University New Taipei City Taiwan 1 Graduate Institute of Clinical Medicine College of Medicine Taipei Medical University Taipei Taiwan 3 Department of Veterinary Medicine National Chung Hsing University Taichung Taiwan 2 School of Gerontology Healthy Management College of Nursing Taipei Medical University Taipei Taiwan 4 Division of Breast Surgery and General Surgery Department of Surgery Cardinal Tien Hospital Xindian District, New Taipei City Taiwan |
AuthorAffiliation_xml | – name: 3 Department of Veterinary Medicine National Chung Hsing University Taichung Taiwan – name: 1 Graduate Institute of Clinical Medicine College of Medicine Taipei Medical University Taipei Taiwan – name: 5 Division of Nephrology Department of Internal Medicine Shuang Ho Hospital Taipei Medical University New Taipei City Taiwan – name: 2 School of Gerontology Healthy Management College of Nursing Taipei Medical University Taipei Taiwan – name: 4 Division of Breast Surgery and General Surgery Department of Surgery Cardinal Tien Hospital Xindian District, New Taipei City Taiwan |
Author_xml | – sequence: 1 givenname: Yuan‐Feng surname: Lin fullname: Lin, Yuan‐Feng organization: Taipei Medical University – sequence: 2 givenname: Ing‐Jy surname: Tseng fullname: Tseng, Ing‐Jy organization: Taipei Medical University – sequence: 3 givenname: Chih‐Jung surname: Kuo fullname: Kuo, Chih‐Jung organization: National Chung Hsing University – sequence: 4 givenname: Hui‐Yu surname: Lin fullname: Lin, Hui‐Yu organization: Cardinal Tien Hospital – sequence: 5 givenname: I‐Jen surname: Chiu fullname: Chiu, I‐Jen organization: Taipei Medical University – sequence: 6 givenname: Hui‐Wen orcidid: 0000-0002-5027-390X surname: Chiu fullname: Chiu, Hui‐Wen email: leu3@tmu.edu.tw organization: Taipei Medical University |
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Copyright | 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. 2018. This work is published under https://creativecommons.org/licenses/by/4.0/ (the "License"). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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Snippet | Paclitaxel‐based chemotherapy is a common strategy to treat patients with triple‐negative breast cancer (TNBC). As paclitaxel resistance is still a clinical... Paclitaxel-based chemotherapy is a common strategy to treat patients with triple-negative breast cancer (TNBC). As paclitaxel resistance is still a clinical... Paclitaxel‐based chemotherapy is a common strategy to treat patients with triple‐negative breast cancer ( TNBC ). As paclitaxel resistance is still a clinical... |
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SubjectTerms | Adult Aged Antineoplastic Combined Chemotherapy Protocols - pharmacology ARID1A Breast cancer Cell Line, Tumor Chemotherapy Disease-Free Survival DNA-Binding Proteins Drug Resistance, Neoplasm - genetics Female Gene Expression Regulation, Neoplastic - drug effects Humans Indoles - pharmacology Kaplan-Meier Estimate Middle Aged Nuclear Proteins - genetics Original p38 Mitogen-Activated Protein Kinases - genetics p38MAPK Paclitaxel Paclitaxel - administration & dosage Paclitaxel - adverse effects Patients Transcription Transcription Factors - genetics Triple Negative Breast Neoplasms - drug therapy Triple Negative Breast Neoplasms - genetics Triple Negative Breast Neoplasms - pathology triple‐negative breast cancer |
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Title | High‐level expression of ARID1A predicts a favourable outcome in triple‐negative breast cancer patients receiving paclitaxel‐based chemotherapy |
URI | https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjcmm.13551 https://www.ncbi.nlm.nih.gov/pubmed/29392887 https://www.proquest.com/docview/2017684150 https://www.proquest.com/docview/1993996407 https://pubmed.ncbi.nlm.nih.gov/PMC5867090 |
Volume | 22 |
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