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Review
. 2015 Jan 20;3(4):e999503.
doi: 10.1080/21623996.2014.999503. eCollection 2014.

Role of STAT3 in lung cancer

Pranabananda Dutta  1 , Nafiseh Sabri  2 , Jinghong Li  1 , Willis X Li  1
Affiliations
Review

Role of STAT3 in lung cancer

Pranabananda Dutta et al. JAKSTAT. .

Abstract

Lung cancer remains a challenging disease. It is responsible for the high cancer mortality rates in the US and worldwide. Elucidation of the molecular mechanisms operative in lung cancer is an important first step in developing effective therapies. Accumulating evidence over the last 2 decades suggests a critical role for Signal Transducer and Activator of Transcription 3 (STAT3) as a point of convergence for various signaling pathways that are dysregulated in the disease. In this review, we discuss possible molecular mechanisms involving STAT3 in lung tumorigenesis based on recent literature. We consider possible roles of STAT3 in cancer cell proliferation and survival, in the tumor immune environment, and in epigenetic regulation and interaction of STAT3 with other transcription factors. We also discuss the potential role of STAT3 in tumor suppression, which complicates strategies of targeting STAT3 in cancer therapy.

Keywords: Non-canonical; U-STAT; immune evasion; miRNA; stem cell; tumor suppressor.

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Figures

Figure 1.
Figure 1.
Role of STAT3 in lung cancer. In lung cancer cells, STAT3 can be activated by EGFR, JAK2, Src, IL6, or others. Negative regulators of STAT3 include SOCS, PIAS, Protein tyrosine phosphatases, and miRNAs. In the canonical pathway, activated STAT3 is phosphorylated at Tyr705 and functions as a transcription factor, inducing downstream target genes that are important for cell proliferation, induction of angiogenesis, prevention of apoptosis, evasion of host immune surveillance, or cancer stem cell self-renewal. Potential non-canonical functions of STAT3 may also operate in lung cancer cells. See text for more details.
See this image and copyright information in PMC

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