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Article

Activation of the HSP27-AKT axis contributes to gefitinib resistance in non-small cell lung cancer cells independent of EGFR mutations.

Cellular oncology (Dordrecht, Netherlands) - 1 Oct 2022

Choi Seul-Ki, Kim Minsuh, Lee Haeseung, Kwon Youngjoo, Cha Hyuk-Jin, Jang Se Jin, Na Younghwa, Lee Yun-Sil

Abstract excerpt

PURPOSE: Although epidermal growth factor receptor (EGFR)-activating mutations in non-small cell lung cancer (NSCLC) usually show sensitivity to first-generation EGFR-tyrosine kinase inhibitors (TKIs), most patients relapse because of drug resistance. Heat shock protein 27 (HSP27) has been reported to be involved in the resistance of EGFR-TKIs, although the underlying mechanism is unclear. Here, we explore the...

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Share to Carcinoma, Non-Small-Cell Lung
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 35931945
DOI: 10.1007/s13402-022-00696-3
PMCID: PMC9579113

Genes

EGFR

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Activation of the HSP27-AKT axis contributes to gefitinib resistance in non-small cell lung cancer cells independent of EGFR mutations.PMID 35931945Read ↗

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