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Monoterpenes Modulating IL-10
Published in Parimelazhagan Thangaraj, Phytomedicine, 2020
Saravanan Shanmugam, Jullyana S. S. Quintans, Parimelazhagan Thangaraj, Luciana Scotti, Marcus T. Scotti, Adriano A. S. Araújo, Lucindo J. Quintans-Júnior
The IL-10/IL-10R signaling pathway. IL-10 signals through the heterotetrameric I-10R complex which is comprised of IL-10Ra (IL-10R1 in humans) and IL-10Rb (IL-10R2 in humans). Binding of IL-10 to its receptor leads to JAK1- and TYK2-mediated phosphorylation of STAT3. The phosphorylation of STAT3 forms drives the expression of anti-inflammatory mediators (Shouval et al. 2014).
Immunology (primary Immunodeficiency Syndromes
Published in Stephan Strobel, Lewis Spitz, Stephen D. Marks, Great Ormond Street Handbook of Paediatrics, 2019
Stephan Strobel, Alison M. Jones
All patients have extremely high IgE levels, varying with age at presentation. Under 1 year IgE may be >1000 IU/ml, but in older patients may be 10,000– 20,000 IU/ml or higher. Patients with severe atopic disease alone may also have very high IgE levels but usually do not exhibit other clinical features of HIES. Other immunology investigations are usually normal, although defects in neutrophil function have been described. The diagnosis is confirmed by demonstration of a mutation in Stat-3.
Early Detection of Chronic Obstructive Pulmonary Disease: Influence on Lung Cancer Epidemiology
Published in Ayman El-Baz, Jasjit S. Suri, Lung Imaging and CADx, 2019
Amany F. Elbehairy, Ahmed Sadaka
A key element in the intracellular signaling pathways in COPD is the transcription factor NF-κB, which upregulates inflammatory mediator expression and activates antiapoptotic proteins, thus increasing cell longevity and the associated risk of mutations and tumorigenesis [38, 53]. The production of NF-κB is also directly stimulated by RNOS found in tobacco smoke. Another proinflammatory signal transducer is the signal transducer and activator of transcription (STAT-3), which is also found to play a major role in COPD inflammation as well as carcinogenesis. Normally, STAT-3 is activated by phosphorylation for a short time span before being quickly dephosphorylated by protein phosphatases. However, in cancerous tissues, aberrant persistent protein activation occurs, where it induces transcription of multiple genes responsible for inhibiting apoptosis, increasing cell proliferation, angiogenesis, and evasion of the body immune system. These are central domains to the process of tumorigenesis [38].
HOTAIR knockdown impairs metastasis of cervical cancer cells by down-regulating metastasis-related genes
Published in Journal of Obstetrics and Gynaecology, 2023
Lei Shi, Dehui Zhang, Huijuan Han, Liangyu Zhang, Sirui Li, Fang Yang, Caijun He
IL6/STAT3 signalling has been shown to drive metastasis in cancers by inducing EMT (Zeng et al.2019). Our results showed that after HOTAIR knockdown, the expression of signal transducer and activator of transcription 3 (STAT3) is significantly downregulated. This might contribute to reduced viability, reduced invasion and migration ability of the cancer cells. Previously, it was shown that miR-411 overexpression leads to reduced STAT3 expression and inhibition of cell proliferation and invasion in cervical cancer (Shan et al.2019). STAT3 is broadly upregulated both in cancer and non-cancerous cells. It inhibits the expression of key immune activators and promotes the synthesis of immunosuppressive factors. Increased STAT3 expression and activation are observed in cervical disease and may play role in cervical carcinogenesis (Morgan et al.2018, Morgan and Macdonald, 2019a). Therefore, whether the downregulation of STAT3 expression after HOTAIR knockdown is associated with the activation of immunosuppressive factors would be an interesting topic for further study.
Ligustrazine inhibits inflammatory response of human endometrial stromal cells through the STAT3/IGF2BP1/RELA axis
Published in Pharmaceutical Biology, 2023
Ying Feng, Han Dong, Liyan Zheng
STAT3 is a crucial member of the STAT3 signaling participates in diverse inflammatory responses and plays an indispensable role in the occurrence of various inflammatory diseases (Chowdhury et al. 2019; Yu et al. 2019). The involvement of STAT3 in the progression of EMs has also been reported. IL-37, an anti-inflammatory cytokine, inhibited the development of EMs in a mouse model by inhibiting STAT3 phosphorylation, while activation of STAT3 effectively reversed IL-37-induced dendritic cell maturation in EMs (Li et al. 2021). Besides, long non-coding RNA AFAP1-AS1 modulated the proliferation and apoptosis of endometrial stromal cells in EMs by activating the STAT3/transforming growth factor-β1/Smad axis (Huan et al. 2021). Consistent with previous literature, our data showed that ligustrazine treatment decreased the phosphorylation level of STAT3 in HESCs, suggesting that ligustrazine may act as an inhibitor of the STAT3 pathway in EMs.
The molecular mechanisms and targeting strategies of transcription factors in cholangiocarcinoma
Published in Expert Opinion on Therapeutic Targets, 2022
Jiao Wang, Fujing Ge, Tao Yuan, Meijia Qian, Fangjie Yan, Bo Yang, Qiaojun He, Hong Zhu
STAT3 participates in the regulation of cell growth, apoptosis, invasion, angiogenesis, and metastasis, and is one of the main mediators of tumorigenesis [41]. STAT3 is the junction of various cytokine pathways, growth factor pathways, and some oncogene-activated signaling pathways. Not only does STAT3 phosphorylation promote ICC metastasis, but STAT3 is also overexpressed in ICC patients [23]. Two independent studies have reported aberrant and sustained activation of the IL6/STAT3 signaling pathway in CCA [10,42]. IL6 contributes to the pathogenesis of CCA by altering the transcription of downstream genes via activating STAT3 phosphorylation, and STAT3 cascade inhibition enhances the sensitivity of CCA cells to trail-mediated apoptosis [10]. Many factors affect the progression of CCA by regulating STAT3, suggesting that STAT3 is a key downstream transcription factor in CCA [10,38,39]. Sorafenib decreases STAT3 phosphorylation by increasing the activity of phosphatase SHP2 and sensitizes CCA cells to TRAIL-mediated apoptosis [39]. Metformin inhibits the proliferation and metastasis of CCA cell lines by inhibiting the nuclear transport of STAT3 [40].