AXL is crucial for E1A-enhanced therapeutic efficiency of EGFR tyrosine kinase inhibitors through NFI in breast cancer

Chih Ming Su; Tung Wei Hsu; Shian Ying Sung; Ming Te Huang; Kuan Chou Chen; Chih Yang Huang; Chien Yi Chiang; Yen Hao Su; Hsin An Chen; Po Hsiang Liao

doi:10.1002/tox.23125

AXL is crucial for E1A-enhanced therapeutic efficiency of EGFR tyrosine kinase inhibitors through NFI in breast cancer

Chih Ming Su, Tung Wei Hsu, Shian Ying Sung, Ming Te Huang, Kuan Chou Chen, Chih Yang Huang, Chien Yi Chiang, Yen Hao Su, Hsin An Chen, Po Hsiang Liao

Research output: Contribution to journal › Article › peer-review

4 Citations (Scopus)

Abstract

AXL which is a chemosensitizer protein for breast cancer cells in response to epidermal growth factor receptor-tyrosine kinase inhibitor and suppresses tumor growth. The clinical information show nuclear factor I (NFI)-C and NFI-X expression correlate with AXL expression in breast cancer patients. Following, we establish serial deletions of AXL promoter to identify regions required for Adenovirus-5 early region 1A (E1A)-mediated AXL suppression. All of the NFI family members were extensively studied for their expression and functions in regulating AXL. Moreover, E1A post-transcriptionally downregulates AXL expression through NFI. NFI-C and NFI-X, not NFI-A and NFI-B, resulting in cell death in response to EGFR-TKI. Our finding suggests that NFI-C and NFI-X are crucial regulators for AXL and significantly correlated with poor survival of breast cancer patients.

Original language	English
Pages (from-to)	1278-1287
Number of pages	10
Journal	Environmental Toxicology
Volume	36
Issue number	7
DOIs	https://doi.org/10.1002/tox.23125
Publication status	Accepted/In press - 2021

Keywords

AXL
breast cancer
EGFR tyrosine kinase inhibitor
nuclear factor I

ASJC Scopus subject areas

Toxicology
Management, Monitoring, Policy and Law
Health, Toxicology and Mutagenesis

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1002/tox.23125

Cite this

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title = "AXL is crucial for E1A-enhanced therapeutic efficiency of EGFR tyrosine kinase inhibitors through NFI in breast cancer",

abstract = "AXL which is a chemosensitizer protein for breast cancer cells in response to epidermal growth factor receptor-tyrosine kinase inhibitor and suppresses tumor growth. The clinical information show nuclear factor I (NFI)-C and NFI-X expression correlate with AXL expression in breast cancer patients. Following, we establish serial deletions of AXL promoter to identify regions required for Adenovirus-5 early region 1A (E1A)-mediated AXL suppression. All of the NFI family members were extensively studied for their expression and functions in regulating AXL. Moreover, E1A post-transcriptionally downregulates AXL expression through NFI. NFI-C and NFI-X, not NFI-A and NFI-B, resulting in cell death in response to EGFR-TKI. Our finding suggests that NFI-C and NFI-X are crucial regulators for AXL and significantly correlated with poor survival of breast cancer patients.",

keywords = "AXL, breast cancer, EGFR tyrosine kinase inhibitor, nuclear factor I",

author = "Su, {Chih Ming} and Hsu, {Tung Wei} and Sung, {Shian Ying} and Huang, {Ming Te} and Chen, {Kuan Chou} and Huang, {Chih Yang} and Chiang, {Chien Yi} and Su, {Yen Hao} and Chen, {Hsin An} and Liao, {Po Hsiang}",

note = "Funding Information: Ministry of Science and Technology grants from Taiwan, Grant/Award Numbers: MOST108‐2314‐B‐038‐109, MOST 109‐2320‐B‐038 ‐043; Taipei Medical University‐Shuang Ho Hospital, Ministry of Health and Welfare grant from Taiwan, Grant/Award Numbers: 103TMU‐SHH‐26, 104TMU‐SHH‐01‐1; TMU Research Center of Cancer Translational Medicine from The Featured Areas Research Center Program within the framework of the Higher Education Sprout Project by the Ministry of Education (MOE) in Taiwan, Grant/Award Numbers: DP2‐110‐21121‐03‐C‐08‐03, DP2‐110‐21121‐03‐C‐08‐01 Funding information Publisher Copyright: {\textcopyright} 2021 Wiley Periodicals LLC.",

year = "2021",

doi = "10.1002/tox.23125",

language = "English",

volume = "36",

pages = "1278--1287",

journal = "Environmental Toxicology",

issn = "1520-4081",

publisher = "John Wiley and Sons Inc.",

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T1 - AXL is crucial for E1A-enhanced therapeutic efficiency of EGFR tyrosine kinase inhibitors through NFI in breast cancer

AU - Su, Chih Ming

AU - Hsu, Tung Wei

AU - Sung, Shian Ying

AU - Huang, Ming Te

AU - Chen, Kuan Chou

AU - Huang, Chih Yang

AU - Chiang, Chien Yi

AU - Su, Yen Hao

AU - Chen, Hsin An

AU - Liao, Po Hsiang

N1 - Funding Information: Ministry of Science and Technology grants from Taiwan, Grant/Award Numbers: MOST108‐2314‐B‐038‐109, MOST 109‐2320‐B‐038 ‐043; Taipei Medical University‐Shuang Ho Hospital, Ministry of Health and Welfare grant from Taiwan, Grant/Award Numbers: 103TMU‐SHH‐26, 104TMU‐SHH‐01‐1; TMU Research Center of Cancer Translational Medicine from The Featured Areas Research Center Program within the framework of the Higher Education Sprout Project by the Ministry of Education (MOE) in Taiwan, Grant/Award Numbers: DP2‐110‐21121‐03‐C‐08‐03, DP2‐110‐21121‐03‐C‐08‐01 Funding information Publisher Copyright: © 2021 Wiley Periodicals LLC.

PY - 2021

Y1 - 2021

N2 - AXL which is a chemosensitizer protein for breast cancer cells in response to epidermal growth factor receptor-tyrosine kinase inhibitor and suppresses tumor growth. The clinical information show nuclear factor I (NFI)-C and NFI-X expression correlate with AXL expression in breast cancer patients. Following, we establish serial deletions of AXL promoter to identify regions required for Adenovirus-5 early region 1A (E1A)-mediated AXL suppression. All of the NFI family members were extensively studied for their expression and functions in regulating AXL. Moreover, E1A post-transcriptionally downregulates AXL expression through NFI. NFI-C and NFI-X, not NFI-A and NFI-B, resulting in cell death in response to EGFR-TKI. Our finding suggests that NFI-C and NFI-X are crucial regulators for AXL and significantly correlated with poor survival of breast cancer patients.

AB - AXL which is a chemosensitizer protein for breast cancer cells in response to epidermal growth factor receptor-tyrosine kinase inhibitor and suppresses tumor growth. The clinical information show nuclear factor I (NFI)-C and NFI-X expression correlate with AXL expression in breast cancer patients. Following, we establish serial deletions of AXL promoter to identify regions required for Adenovirus-5 early region 1A (E1A)-mediated AXL suppression. All of the NFI family members were extensively studied for their expression and functions in regulating AXL. Moreover, E1A post-transcriptionally downregulates AXL expression through NFI. NFI-C and NFI-X, not NFI-A and NFI-B, resulting in cell death in response to EGFR-TKI. Our finding suggests that NFI-C and NFI-X are crucial regulators for AXL and significantly correlated with poor survival of breast cancer patients.

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KW - EGFR tyrosine kinase inhibitor

KW - nuclear factor I

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AXL is crucial for E1A-enhanced therapeutic efficiency of EGFR tyrosine kinase inhibitors through NFI in breast cancer

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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