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Review
. 2020 Jan 1;11(4):837-848.
doi: 10.7150/jca.35011. eCollection 2020.

STAT3 signaling in ovarian cancer: a potential therapeutic target

Affiliations
Review

STAT3 signaling in ovarian cancer: a potential therapeutic target

Renba Liang et al. J Cancer. .

Abstract

Accumulating evidence has shown that Signal Transducer and Activator of Transcription 3 (STAT3) is thought to be a promising target for cancer therapy as STAT3 is frequently overexpressed in a wide range of cancer cells as well as clinical specimens, promoting tumor progression. It is widely accepted that STAT3 regulates a variety of cellular processes, such as tumor cell growth, survival, invasion, cancer stem cell-like characteristic, angiogenesis and drug-resistance. In this review, we focus on the role of STAT3 in tumorigenesis in ovarian cancer and discuss the existing inhibitors of STAT3 signaling that can be promisingly developed as the strategies for ovarian cancer therapy.

Keywords: STAT3; inhibitors; ovarian cancer; tumorigenesis.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interest exists.

Figures

Figure 1
Figure 1
Linear topology of STAT3 structure. As shown, STAT3 is made up of the N-terminal domain, the coiled-coil domain, the DNA binding domain (DBD), the linker domain, the Src-homology 2(SH2) domain, and the C-terminal domain. The tyrosine residue at position 705 (Tyr-705) is close to SH2 domain.
Figure 2
Figure 2
The abnormal activation of STAT3 signaling in ovarian cancer. In ovarian cancer, STAT3 is activated via phosphorylation of Tyr-705 by growth factor receptor tyrosine kinases, cytokine receptor associated kinases (JAK), and non-receptor kinases (Src). After activation, STAT3 forms dimerization and translocate into nucleus, in which they bind to promoter of STAT3-targeted genes, resulting in gene transcription.
Figure 3
Figure 3
STAT3-targeted genes and their role in tumorigenesis/progress. Persistent activation of STAT3 promotes its-regulated genes expression, which contribute to ovarian cancer growth, survival, invasion, angiogenesis, stem cell-like characteristic, and chemo-resistance.
Figure 4
Figure 4
Chemical structures of natural inhibitors of STAT3 in ovarian cancer.

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