JAK-STAT signaling pathway and its inhibitors in the treatment of atopic dermatitis

Abstract:: Breast cancer is the most common malignant tumor in women worldwide. Traditional ways of treatment, includ-ing radiotherapy and endocrine therapy, for breast cancer have inevitable side effects. In recent decades, targeted therapies for breast cancer have rapidly advanced and shown a promising future. The JAK/STAT signaling pathway has been shown to play important roles in tumorigenesis, maintenance and metastasis of breast cancer. Hence, many small molecule inhibi-tors of JAK and STAT proteins have been developed. These inhibitors exhibit potent inhibitory effects on breast cancer in both cellular and animal models, and even some of them have already been in clinical trials. This review article discussed the JAK/STAT signal transduction pathway in the pathogenesis of breast cancer, and the potential for the application of JAK/STAT inhibitors in breast cancer treatment.

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IFN-γ inhibits ovarian cancer progression via SOCS1/JAK/STAT signaling pathway

Clinical & Translational Oncology ◽

10.1007/s12094-021-02668-9 ◽

2021 ◽

Author(s):

A. H. Gao ◽

Y. R. Hu ◽

W. P. Zhu

Keyword(s):

Ovarian Cancer ◽

Signaling Pathway ◽

Cancer Progression ◽

Stat Signaling ◽

Ifn Γ

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Preparation of T-2-glucoronide with Rat Hepatic Microsomes and Its Use along with T-2 for Activation of the JAK/STAT Signaling Pathway in RAW264.7 Cells

Journal of Agricultural and Food Chemistry ◽

10.1021/acs.jafc.7b01250 ◽

2017 ◽

Vol 65 (23) ◽

pp. 4811-4818 ◽

Cited By ~ 3

Author(s):

Xing Wang ◽

Yaling Wang ◽

Yapei Wang ◽

Lijun Sun ◽

Ravi Gooneratne

Keyword(s):

Signaling Pathway ◽

Raw264.7 Cells ◽

Hepatic Microsomes ◽

Stat Signaling

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Kyungheechunggan-Tang-01, a New Herbal Medication, Suppresses LPS-Induced Inflammatory Responses through JAK/STAT Signaling Pathway in RAW 264.7 Macrophages

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2017/7383104 ◽

2017 ◽

Vol 2017 ◽

pp. 1-15 ◽

Cited By ~ 4

Author(s):

Hee-Soo Han ◽

Eungyeong Jang ◽

Ji-Sun Shin ◽

Kyung-Soo Inn ◽

Jang-Hoon Lee ◽

...

Keyword(s):

Signaling Pathway ◽

Inflammatory Responses ◽

Inflammatory Diseases ◽

Molecular Data ◽

Mrna Levels ◽

Protein Levels ◽

Stat3 Phosphorylation ◽

Stat Signaling ◽

Cox 2 ◽

Anti Inflammatory

Medicinal plants have been used as alternative therapeutic tools to alleviate inflammatory diseases. The objective of this study was to evaluate anti-inflammatory properties of Kyungheechunggan-tang- (KCT-) 01, KCT-02, and Injinchunggan-tang (IJCGT) as newly developed decoctions containing 3–11 herbs in LPS-induced macrophages. KCT-01 showed the most potent inhibitory effects on LPS-induced NO, PGE2, TNF-α, and IL-6 production among those three herbal formulas. In addition, KCT-01 significantly inhibited LPS-induced iNOS and COX-2 at protein levels and expression of iNOS, COX-2, TNF-α, and IL-6 at mRNA levels. Molecular data revealed that KCT-01 attenuated the activation of JAK/STAT signaling cascade without affecting NF-κB or AP-1 activation. In ear inflammation induced by croton oil, KCT-01 significantly reduced edema, MPO activity, expression levels of iNOS and COX-2, and STAT3 phosphorylation in ear tissues. Taken together, our findings suggest that KCT-01 can downregulate the expression of proinflammatory genes by inhibiting JAK/STAT signaling pathway under inflammatory conditions. This study provides useful data for further exploration and application of KCT-01 as a potential anti-inflammatory medicine.

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Analysis of JAK-STAT signaling pathway genes and their microRNAs in the intestinal mucosa of genetically disparate chicken lines induced with necrotic enteritis

Veterinary Immunology and Immunopathology ◽

10.1016/j.vetimm.2017.03.001 ◽

2017 ◽

Vol 187 ◽

pp. 1-9 ◽

Cited By ~ 7

Author(s):

Anh Duc Truong ◽

Deivendran Rengaraj ◽

Yeojin Hong ◽

Cong Thanh Hoang ◽

Yeong Ho Hong ◽

...

Keyword(s):

Signaling Pathway ◽

Intestinal Mucosa ◽

Necrotic Enteritis ◽

Stat Signaling

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Constitutive activation of STAT-3 and downregulation of SOCS-3 expression induced by adrenalectomy

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.2001.281.6.r2048 ◽

2001 ◽

Vol 281 (6) ◽

pp. R2048-R2058 ◽

Cited By ~ 24

Author(s):

Abram M. Madiehe ◽

Ling Lin ◽

Christy White ◽

H. Doug Braymer ◽

George A. Bray ◽

...

Keyword(s):

Dna Binding ◽

Signaling Pathway ◽

Leptin Receptor ◽

Binding Activity ◽

Janus Kinase ◽

Adrenal Steroids ◽

Western Blots ◽

Protein Levels ◽

Dna Binding Activity ◽

Stat Signaling

Removal of adrenal steroids by adrenalectomy (ADX) slows or reverses the development of many forms of obesity in rodents, including those that are leptin or leptin receptor deficient. Obesity is associated with hyperleptinemia and leptin resistance. We hypothesized that glucocorticoids impair leptin receptor signaling and that removal thereof would activate the Janus kinase (JAK)-signal transducers and activators of transcription (STAT) signaling pathway. The inhibitory effect of leptin (2.5 μg icv) on food intake was enhanced in ADX rats. A combination of ribonuclease protection assays, RT-PCR, Western blots, and mobility shift assays was used to evaluate the leptin signaling pathway in whole hypothalami from sham-operated, ADX and corticosterone-replaced ADX (ADX-R) Sprague-Dawley rats that were treated acutely with either saline vehicle or leptin intracerebroventricularly. ADX increased the expression of leptin receptor mRNA, increased STAT-3 mRNA and protein levels, induced constitutive STAT-3 phosphorylation and DNA binding activity, and also reduced suppressor of cytokine signaling-3 (SOCS-3) mRNA and protein levels. ADX and leptin treatment increased STAT-3 phosphorylation, but with no concomitant increase in DNA binding activity. Leptin and ADX decreased NPY mRNA expression, but their combination did not further decrease NPY mRNA. Corticosterone supplementation of ADX rats partially reversed many of these effects. In conclusion, ADX through activation of STAT-3 and inhibition of SOCS-3 activates the JAK-STAT signaling pathway. These effects most probably explain the ability to prevent the development of obesity by removal of adrenal steroids.

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