The Role of STAT3 in Non-Small Cell Lung Cancer

Cancers

Daijiro Harada¹  Nagio Takigawa² 

[1] Department of Thoracic Oncology, NHO Shikoku Cancer Center, 160 Minami-Umemoto-cho, Matsuyama 791-0280, Japan; E-Mail:;Department of General Internal Medicine 4, Kawasaki Medical School, 2-1-80 Nakasange, Kita-ku, Okayama 700-8505, Japan

关键词: signal transducer and activator of transcription 3;    Janus kinase 2;    epidermal growth factor receptor;    non-small cell lung cancer;    drug resistance;   

DOI  :  10.3390/cancers6020708

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland.