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Article

Dioscin overcome TKI resistance in EGFR-mutated lung adenocarcinoma cells via down-regulation of tyrosine phosphatase SHP2 expression.

International journal of biological sciences - 1 Jan 2018

Wang Yao-Chen, Wu De-Wei, Wu Tzu-Chin, Wang Lee, Chen Chih-Yi, Lee Huei

Abstract excerpt

Resistance to tyrosine kinase inhibitors (TKIs) results in tumor relapse and poor prognosis in patients with lung adenocarcinoma. TKI resistance caused by epidermal growth factor receptor (EGFR) mutations at T790M and c-Met amplification occurs through persistent activation of the MEK/ERK and PI3K/AKT signaling pathways. We therefore expected that dual inhibitors of both signaling pathways could overcome TKI...

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Share to Adaptor Proteins, Signal Transducing
Share to Adenocarcinoma of Lung

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Chromatin Immunoprecipitation

Share to Drug Resistance, Neoplasm

Share to Enzyme Inhibitors

Share to Gene Expression Regulation, Enzymologic

Share to Protein Tyrosine Phosphatase, Non-Receptor Type 11

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Source

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Identifiers

PMID: 29483824
DOI: 10.7150/ijbs.22209
PMCID: PMC5821048

Genes

EGFR
GAB1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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