Identification of STAT3-independent regulatory effects for protein inhibitor of activated STAT3 by binding to novel transcription factors

Dabir, Snehal; Kluge, Amy; Aziz, Mehar; Houghton, Janet A.; Dowlati, Afshin

doi:10.4161/cbt.12.2.15732

Cited by 9 publications

(8 citation statements)

References 29 publications

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“…Congenital cystic adenomatoid malformation (CCAM) type II of the lung has been reported in two individuals with large, BP1/2-BP4 deletions (subject 32 here and patient 17 in Brunetti-Pierri et al 4 ). As CCAM is likely because of the focal arrest in lung maturation during the fetal period, 38 candidate genes for this malformation include genes with roles in developmental pathways, including PIAS3 and RBM8A, which regulate STAT3, 39,40 involved in lung branching morphogenesis; 41 BCL9, which is involved in the b-catenin/WNT pathway, 42 also active in the lung development; 43 and PEX11B, which encodes a peroxisome biogenesis factor hypothesized to be important in developing airways and during alveolarization. 44 There have been multiple reports of polydactyly associated with the distal, BP3-BP4 microdeletion (Table 1).…”

Section: Discussionmentioning

confidence: 99%

Proximal microdeletions and microduplications of 1q21.1 contribute to variable abnormal phenotypes

et al. 2012

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Chromosomal band 1q21.1 can be divided into two distinct regions, proximal and distal, based on segmental duplications that mediate recurrent rearrangements. Microdeletions and microduplications of the distal region within 1q21.1, which are susceptibility factors for a variety of neurodevelopmental phenotypes, have been more extensively studied than proximal microdeletions and microduplications. Proximal microdeletions are known as a susceptibility factor for thrombocytopenia-absent radius (TAR) syndrome, but it is unclear if these proximal microdeletions have other phenotypic consequences. Therefore, to elucidate the clinical significance of rearrangements of the proximal 1q21.1 region, we evaluated the phenotypes in patients identified with 1q21.1 rearrangements after referral for clinical microarray testing. We report clinical information for 55 probands with copy number variations (CNVs) involving proximal 1q21.1: 22 microdeletions and 20 reciprocal microduplications limited to proximal 1q21.1 and 13 microdeletions that include both the proximal and distal regions. Six individuals with proximal microdeletions have TAR syndrome. Three individuals with proximal microdeletions and two individuals with larger microdeletions of proximal and distal 1q21.1 have a 'partial' TAR phenotype. Furthermore, one subject with TAR syndrome has a smaller, atypical deletion, narrowing the critical deletion region for the syndrome. Otherwise, phenotypic features varied among individuals with these microdeletions and microduplications. The recurrent, proximal 1q21.1 microduplications are enriched in our population undergoing genetic testing compared with control populations. Therefore, CNVs in proximal 1q21.1 can be a contributing factor for the development of abnormal phenotypes in some carriers

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Section: Discussionmentioning

confidence: 99%

Proximal microdeletions and microduplications of 1q21.1 contribute to variable abnormal phenotypes

et al. 2012

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“…A previous study showed that PIAS3 overexpression in breast cancer cell lines can significantly modulate STAT5-mediated gene expression and induce cellular apoptosis [24]. In addition, PIAS3 has a vast STAT3-independent effect by binding to a number of transcription factors with downstream alterations in apoptosis, angiogenesis, and a number of signaling pathways, for instance, it interacts with nuclear hormone receptors, androgen receptors, estrogen receptors, p53, BRCA1, and metastasis tumor antigen [25].…”

Section: Discussionmentioning

confidence: 99%

The role of protein inhibitor of activated STAT3 and miRNA-18a expressions in breast cancer

Nomair

Ahmed

Nomeir

et al. 2019

Egypt J Med Hum Genet

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Background: Breast cancer is a disease characterized by progressive genetic abnormalities including mutations in tumor suppressor genes and oncogenes, as well as other chromosomal abnormalities. Protein inhibitor of activated signal transducer and activator of transcription 3 (PIAS3) is a member of the PIAS family of transcriptional modulators; its expression is altered in many cancers. Micro-ribonucleic acid (miRNA)-18a acts as an oncogene by negatively regulating PIAS3 and thus modulating the expression of signal transducer and activator of transcription 3 (STAT3) target genes. The aim of this work is to examine the expression levels of PIAS3 gene and miRNA-18a in breast cancer tissues and nearby non-tumor tissues. The samples of breast cancer and paired samples of noncancerous tissue from the same resected breast were obtained from 25 patients undergoing surgery. Full history taking, complete physical examination, pre-operative fine-needle aspiration cytology or ultrasonic (U/S)-guided core biopsy from the breast mass, final surgical biopsy for pathological examination, and routine laboratory investigations were done. Estrogen receptors (ER), progesterone receptors (PR), and human epidermal growth factor receptor 2 (HER2) status were evaluated. Total RNA extraction followed by real-time reverse transcriptionpolymerase chain reaction (RT-PCR) for quantification of PIAS3 mRNA and miRNA-18a expressions was performed. Results: The mean value of PIAS3 mRNA fold expression was significantly lower in the tumor group (5.12 ± 9.85) compared to the normal group (8.38 ± 17.10) (p = 0.040). miRNA-18a fold expression was higher among tumor group (3.5 ± 7.4) than that of normal group (2.5 ± 3), however, it did not reach the level of statistical significance (p = 0.861). miRNA-18a fold expression had negative significant correlation with PIAS3 mRNA fold expression (p = 0.018). A significant association was observed between miRNA-18a expression in breast cancer tissues and the pathological grade of the tumor (p = 0.029). Conclusions: The results of this study showed that PIAS3 mRNA and miRNA-18a might be of importance in breast cancer development and pathogenesis, and this may be reflected on the treatment strategies targeting STAT3 pathway. However, further studies with larger sample size are needed to validate these observations.

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“…PIAS3 is an endogenous inhibitor of STAT3 and has antiproliferative properties. Glioblastoma and squamous cell lung cancer lack PIAS3 expression (Dabir et al 2011). PIAS3 can affect the growth of cancer cells by inhibiting the JAK/STAT and PI3-K/Akt signaling pathways or regulating its SUMO (small-ubiquitin like modifiers) ligase activity in some malignancy (Liu et al 2011).…”

Section: Discussionmentioning

confidence: 99%

Association of Sedentary Behavior with the Expression Levels of Biomarkers in Colorectal Cancer: Clinical Analysis of 228 Patients

Takata

Lü

et al. 2014

Tohoku J. Exp. Med.

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There is an association between sedentary behavior and the risk of colorectal cancer (CRC), but the underlying mechanism is unclear. CRC is characterized by the changes in the expression levels of biomarkers, including voltage-gated proton channel Hv1, matrix-remodeling associated 5 (MXRA5), DEK (inducing positive supercoils into circular DNA) and protein inhibitor of activated signal transducer and activators of transcription 3 (PIAS3). Thus, sedentary behavior may affect the expression levels of these biomarkers in the colorectal tissue. Here, we recruited 228 CRC patients (128 males, 57.8 ± 7.8 years; 100 females, 57.7 ± 7.5 years) and 80 healthy subjects (48 males, 57.5 ± 6.8 years; 32 females, 56.9 ± 6.5 years) from March 7th, 2010 to May 6th, 2012. All the subjects were unrelated Han Chinese with the similar cultural and economic background. All the subjects were interviewed concerning sedentary time (sitting time categories: less than 1, 1-3, 4-6, and more than 6 h/day). The daily sedentary time of most CRC patients was more than 4 h/day, while the sedentary time of most healthy subjects was less than 3 h/ day. The expression levels of Hv1, MXRA5 and DEK mRNAs and proteins were higher in CRC tissues and the levels of PIAS3 mRNA and protein were lower when the daily sedentary time was longer in CRC patients (p < 0.05). The daily sedentary time was correlated with the protein levels of CRC biomarkers. Furthermore, the sedentary time was positively related with body mass index but not daily calorie intake.

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Identification of STAT3-independent regulatory effects for protein inhibitor of activated STAT3 by binding to novel transcription factors

Cited by 9 publications

References 29 publications

Proximal microdeletions and microduplications of 1q21.1 contribute to variable abnormal phenotypes

Proximal microdeletions and microduplications of 1q21.1 contribute to variable abnormal phenotypes

The role of protein inhibitor of activated STAT3 and miRNA-18a expressions in breast cancer

Association of Sedentary Behavior with the Expression Levels of Biomarkers in Colorectal Cancer: Clinical Analysis of 228 Patients

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