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Concomitant gain of pSTAT3 Tyr705 and loss of PIAS3 appear critical for initiation and development of high-grade serous carcinoma.
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Study reports that SMAD6 is overexpressed in nuclei of glioma cells, which correlates with poor patient survival and regulates STAT3 activity via negatively regulating PIAS3. Mechanically, SMAD6 interacts directly with PIAS3, and this interaction is mediated through the Mad homology 2 domain of SMAD6 and the Ring domain of PIAS3.
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PAI-1 interacted with PIAS3 to regulate Stat3-dependent gene expression and miR-34a was transcriptionally suppressed by Stat3 to form a positive regulatory loop through Stat3 signaling in non-small cell lung cancer cells.
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Levels of PIAS3 are significantly lower, in contrast with phosphorylation of STAT3, in women with endometriosis compared to women without endometriosis.
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TRIM8 activates STAT3 by suppressing the expression of PIAS3, an inhibitor of STAT3, most likely through E3-mediated ubiquitination and proteasomal degradation.
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Low PIAS3 expression is associated with breast cancer organoid invasiveness.
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SHP2, SOCS3 and PIAS3 levels are reduced in medulloblastomas in vivo and in vitro, of which PIAS3 downregulation is more reversely correlated with STAT3 activation. In resveratrol-suppressed medulloblastoma cells with STAT3 downregulation and decreased incidence of STAT3 nuclear translocation, PIAS3 is upregulated, the SHP2 level remains unchanged and SOCS3 is downregulated.
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The results revealed that although the expression levels of SOCS1, SOCS3 and, in particular, pSHP2, tend to decrease in the four types of astrocytomas, PIAS3 downregulation is more negatively correlated with STAT3 activation in the stepwise progress of astrocytomas and would indicate an unfavorable outcome.
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3-Formylchromone inhibits proliferation and induces apoptosis of multiple myeloma cells by abrogating STAT3 signaling through the induction of PIAS3.
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PIAS3 may serve as a biomarker for predicting hormone therapy stratification, although it is limited to those breast cancer patients receiving hormone therapy.
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Taken together, these results suggest that PIAS3 functions as a positive regulator of HIF-1alpha-mediated transcription by increasing its protein stability.
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PIAS3 suppression may be protective against joint destruction in rheumatoid arthritis by regulating synoviocyte migration, invasion, and activation.
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PIAS3 primes ATR for checkpoint activation.
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PIAS3 expression in squamous cell lung cancer is low and predicts overall survival
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Adenovirus E4-ORF3 targets PIAS3 and together with E1B-55K remodels SUMO2/SUMO3 Interactions in the nucleus and at virus genome replication domains.
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Statistically significant positive correlation has been found between STAT5B and COX-2, and significant negative correlation between STAT5B and PIAS3.
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Low PIAS3 expression in malignant mesothelioma is associated with increased STAT3 activation and poor patient survival.
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this newly identified p53PIAS3 interaction through the 1-52 amino acid region of p53, reduces p53MDM2 complex formation, which not only increases the half-life of p53, but also its transactivation of target genes.
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PIAS3 may be a potential biomarker target for early cancer detection and therapeutic of human colorectal cancer.
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PIAS3 activates the intrinsic apoptotic pathway in non-small cell lung cancer cells independent of p53 status.
