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Article

Dual inhibition of MEK1/2 and EGFR synergistically induces caspase-3-dependent apoptosis in EGFR inhibitor-resistant lung cancer cells via BIM upregulation.

Investigational new drugs - 1 Dec 2013

Song Ji-Young, Kim Choung-Soo, Lee Je-Hwan, Jang Se Jin, Lee Sang-wook, Hwang Jung Jin, Lim Chulsoo, Lee Gilnam, Seo Jeongbeob, Cho Suk Young, Choi Jene

Abstract excerpt

Epidermal growth factor receptor (EGFR) gene mutations activate the KRAS-RAF-MEK-ERK pathway in lung cancer cells. EGFR tyrosine kinase inhibitors (TKIs) such as gefitinib induce apoptosis of cancer cells, but prolonged treatment is often associated with acquired resistance. Here, we identified a novel MEK1/2 inhibitor, CZ0775, and compared its cytotoxic effects to those of AZD6244 (selumetinib) in non-small cell...

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Identifiers

PMID: 24068620
DOI: 10.1007/s10637-013-0030-0

Genes

EGFR
KRAS

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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.

Related research

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Dual inhibition of MEK1/2 and EGFR synergistically induces caspase-3-dependent apoptosis in EGFR inhibitor-resistant lung cancer cells via BIM upregulation.PMID 24068620Read ↗

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Combined use of PI3K and MEK inhibitors synergistically inhibits lung cancer with EGFR and KRAS mutations.Semantic proximity Read ↗

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Novel Dual-Target Kinase Inhibitors of EGFR and ALK Were Designed, Synthesized, and Induced Cell Apoptosis in Non-Small Cell Lung Cancer.Semantic proximity Read ↗

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