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<p>Lung adenocarcinoma (LUAD) with epidermal growth factor receptor (EGFR) mutations is prevalent in East Asian NSCLC patients and responds initially to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), but resistance inevitably develops. This study identifies ATP-binding cassette subfamily A member 3 (ABCA3) as a key protein involved in tumor progression and TKI resistance in EGFR-mutant cancers. ABCA3 was significantly upregulated in EGFR-mutant LUAD cells compared to WT, promoting cell viability, proliferation, migration, and clonogenicity, while suppressing apoptosis. Mechanistic analyses revealed that ABCA3 enhanced cholesterol uptake and activated the PI3K/AKT/mTOR pathway, contributing to tumor growth. Moreover, the transcription factor SP1 was found to induce ABCA3 expression, especially following EGFR-TKI treatment. ABCA3 was markedly elevated in EGFR-TKI-resistant cell line, and its inhibition restored drug sensitivity. These findings suggest that ABCA3 plays a central role in mediating both tumor progression and resistance in EGFR-mutant LUAD. Targeting ABCA3 may represent a promising strategy to suppress tumor growth and overcome EGFR-TKI resistance, providing a novel therapeutic avenue for patients with EGFR-mutated non-small cell lung cancer.</p>

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Targeting ABCA3 impedes tumor progression and EGFR-TKI resistance in EGFR-mutant LUAD

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月10日

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  • Zhexian Chen,
  • Guanting Li,
  • Jianyuan Yang,
  • Zimo Chen,
  • Xu Guo,
  • Liang Zhu,
  • Chao Zhou,
  • Yuqing Liu

摘要

Lung adenocarcinoma (LUAD) with epidermal growth factor receptor (EGFR) mutations is prevalent in East Asian NSCLC patients and responds initially to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), but resistance inevitably develops. This study identifies ATP-binding cassette subfamily A member 3 (ABCA3) as a key protein involved in tumor progression and TKI resistance in EGFR-mutant cancers. ABCA3 was significantly upregulated in EGFR-mutant LUAD cells compared to WT, promoting cell viability, proliferation, migration, and clonogenicity, while suppressing apoptosis. Mechanistic analyses revealed that ABCA3 enhanced cholesterol uptake and activated the PI3K/AKT/mTOR pathway, contributing to tumor growth. Moreover, the transcription factor SP1 was found to induce ABCA3 expression, especially following EGFR-TKI treatment. ABCA3 was markedly elevated in EGFR-TKI-resistant cell line, and its inhibition restored drug sensitivity. These findings suggest that ABCA3 plays a central role in mediating both tumor progression and resistance in EGFR-mutant LUAD. Targeting ABCA3 may represent a promising strategy to suppress tumor growth and overcome EGFR-TKI resistance, providing a novel therapeutic avenue for patients with EGFR-mutated non-small cell lung cancer.