Cancers 2014, 6(2), 708-722; doi:10.3390/cancers6020708

The Role of STAT3 in Non-Small Cell Lung Cancer

1email, 2,* email and 3email
Received: 5 December 2013; in revised form: 23 February 2014 / Accepted: 7 March 2014 / Published: 26 March 2014
(This article belongs to the Special Issue STAT3 Signalling in Cancer: Friend or Foe)
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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.
Keywords: signal transducer and activator of transcription 3; Janus kinase 2; epidermal growth factor receptor; non-small cell lung cancer; drug resistance
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MDPI and ACS Style

Harada, D.; Takigawa, N.; Kiura, K. The Role of STAT3 in Non-Small Cell Lung Cancer. Cancers 2014, 6, 708-722.

AMA Style

Harada D, Takigawa N, Kiura K. The Role of STAT3 in Non-Small Cell Lung Cancer. Cancers. 2014; 6(2):708-722.

Chicago/Turabian Style

Harada, Daijiro; Takigawa, Nagio; Kiura, Katsuyuki. 2014. "The Role of STAT3 in Non-Small Cell Lung Cancer." Cancers 6, no. 2: 708-722.

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