The role of STAT3 in non-small cell lung cancer

Daijiro Harada, Nagio Takigawa, Katsuyuki Kiura

Research output: Contribution to journalReview article

80 Citations (Scopus)

Abstract

Persistent phosphorylation of signal transducer and activator of transcription 3 (STAT3) has been demonstrated in 22%~65% of non-small cell lung cancers (NSCLC). STAT3 activation is mediated by receptor tyrosine kinases, such as epidermal growth factor receptor (EGFR) and MET, cytokine receptors, such as IL-6, and non-receptor kinases, such as Src. Overexpression of total or phosphorylated STAT3 in resected NSCLC leads to poor prognosis. In a preclinical study, overexpression of STAT3 was correlated with chemoresistance and radioresistance in NSCLC cells. Here, we review the role of STAT3 and the mechanisms of treatment resistance in malignant diseases, especially NSCLC. As STAT3 is a critical mediator of the oncogenic effects of EGFR mutations, we discuss STAT3 pathways in EGFR-mutated NSCLC, referring to mechanisms of EGFR tyrosine kinase inhibitor resistance.

Original languageEnglish
Pages (from-to)708-722
Number of pages15
JournalCancers
Volume6
Issue number2
DOIs
Publication statusPublished - Jun 2014

Keywords

  • Drug resistance
  • Epidermal growth factor receptor
  • Janus kinase 2
  • Non-small cell lung cancer
  • Signal transducer and activator of transcription 3

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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