YTHDF3 Modulates EGFR/ATK/ERK/p21 Signaling Axis to Promote Cancer Progression and Osimertinib Resistance of Glioblastoma Cells

Hsun Hua Lee; Ching Chuan Hsieh; Cheng Chih Chang; Wan Ting Liao; Hsiang Cheng Chi

doi:10.21873/anticanres.16751

YTHDF3 Modulates EGFR/ATK/ERK/p21 Signaling Axis to Promote Cancer Progression and Osimertinib Resistance of Glioblastoma Cells

Hsun Hua Lee, Ching Chuan Hsieh, Cheng Chih Chang, Wan Ting Liao, Hsiang Cheng Chi

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

1 Citation (Scopus)

Abstract

Background/Aim: Despite recent advances in EGFR-tyrosine kinase inhibitor (TKI) drugs for glioblastoma multiforme (GBM), intrinsic EGFR alterations in GBM have resulted in drug resistance and unsatisfactory clinical development of EGFR-TKIs. Determining the unknown mechanisms underlying EGFR-TKI drug resistance is an urgent, but unmet, medical need for GBM. Although several m⁶A RNA methylation regulators, such as reader YTHDF1/2, were recently predicted to be related to GBM recurrence, none was associated with resistance to the 3^rd generation EGFR-TKI osimertinib.

Original language	English
Pages (from-to)	5485-5498
Number of pages	14
Journal	Anticancer Research
Volume	43
Issue number	12
DOIs	https://doi.org/10.21873/anticanres.16751
Publication status	Published - 2023

Keywords

EGFR
GBM
Osimertinib
Osimertinib resistance
p21
senescence
stemness
YTHDF3

ASJC Scopus subject areas

Oncology
Cancer Research

UN SDGs

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

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10.21873/anticanres.16751

Cite this

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title = "YTHDF3 Modulates EGFR/ATK/ERK/p21 Signaling Axis to Promote Cancer Progression and Osimertinib Resistance of Glioblastoma Cells",

abstract = "Background/Aim: Despite recent advances in EGFR-tyrosine kinase inhibitor (TKI) drugs for glioblastoma multiforme (GBM), intrinsic EGFR alterations in GBM have resulted in drug resistance and unsatisfactory clinical development of EGFR-TKIs. Determining the unknown mechanisms underlying EGFR-TKI drug resistance is an urgent, but unmet, medical need for GBM. Although several m6A RNA methylation regulators, such as reader YTHDF1/2, were recently predicted to be related to GBM recurrence, none was associated with resistance to the 3rd generation EGFR-TKI osimertinib.",

keywords = "EGFR, GBM, Osimertinib, Osimertinib resistance, p21, senescence, stemness, YTHDF3",

author = "Lee, {Hsun Hua} and Hsieh, {Ching Chuan} and Chang, {Cheng Chih} and Liao, {Wan Ting} and Chi, {Hsiang Cheng}",

year = "2023",

doi = "10.21873/anticanres.16751",

language = "English",

volume = "43",

pages = "5485--5498",

journal = "Anticancer Research",

issn = "0250-7005",

publisher = "International Institute of Anticancer Research",

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}

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T1 - YTHDF3 Modulates EGFR/ATK/ERK/p21 Signaling Axis to Promote Cancer Progression and Osimertinib Resistance of Glioblastoma Cells

AU - Lee, Hsun Hua

AU - Hsieh, Ching Chuan

AU - Chang, Cheng Chih

AU - Liao, Wan Ting

AU - Chi, Hsiang Cheng

PY - 2023

Y1 - 2023

N2 - Background/Aim: Despite recent advances in EGFR-tyrosine kinase inhibitor (TKI) drugs for glioblastoma multiforme (GBM), intrinsic EGFR alterations in GBM have resulted in drug resistance and unsatisfactory clinical development of EGFR-TKIs. Determining the unknown mechanisms underlying EGFR-TKI drug resistance is an urgent, but unmet, medical need for GBM. Although several m6A RNA methylation regulators, such as reader YTHDF1/2, were recently predicted to be related to GBM recurrence, none was associated with resistance to the 3rd generation EGFR-TKI osimertinib.

AB - Background/Aim: Despite recent advances in EGFR-tyrosine kinase inhibitor (TKI) drugs for glioblastoma multiforme (GBM), intrinsic EGFR alterations in GBM have resulted in drug resistance and unsatisfactory clinical development of EGFR-TKIs. Determining the unknown mechanisms underlying EGFR-TKI drug resistance is an urgent, but unmet, medical need for GBM. Although several m6A RNA methylation regulators, such as reader YTHDF1/2, were recently predicted to be related to GBM recurrence, none was associated with resistance to the 3rd generation EGFR-TKI osimertinib.

KW - EGFR

KW - GBM

KW - Osimertinib

KW - Osimertinib resistance

KW - p21

KW - senescence

KW - stemness

KW - YTHDF3

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YTHDF3 Modulates EGFR/ATK/ERK/p21 Signaling Axis to Promote Cancer Progression and Osimertinib Resistance of Glioblastoma Cells

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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