scholarly journals Tanshinone I inhibits the growth and metastasis of osteosarcoma via suppressing JAK/STAT3 signalling pathway

2019 ◽  
Vol 23 (9) ◽  
pp. 6454-6465 ◽  
Author(s):  
Weiguo Wang ◽  
Jinsong Li ◽  
Zhiyu Ding ◽  
Yuezhan Li ◽  
Jianlong Wang ◽  
...  
Keyword(s):  
Signalling Pathway ◽  
Tanshinone I ◽  
Stat3 Signalling

Human omental adipose-derived mesenchymal stem cells enhance autophagy in ovarian carcinoma cells through the STAT3 signalling pathway

2020 ◽  
Vol 69 ◽  
pp. 109549 ◽  
Author(s):  
Yijing Chu ◽  
Yan Wang ◽  
Kun Li ◽  
Meixin Liu ◽  
Yan Zhang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Ovarian Carcinoma ◽  
Carcinoma Cells ◽  
Signalling Pathway ◽  
Ovarian Carcinoma Cells ◽  
Stat3 Signalling

scholarly journals PO-183 Prolactin activation of JAK2/STAT3 signalling pathway through GHR in NSCLC

2018 ◽  
Author(s):  
JC Chou ◽  
PS Wang ◽  
SW Wang ◽  
H Lin
Keyword(s):  
Signalling Pathway ◽  
Stat3 Signalling

scholarly journals Myeloid‐derived suppressor cells promote epithelial ovarian cancer cell stemness by inducing the CSF2/p‐STAT3 signalling pathway

FEBS Journal ◽  
2020 ◽  
Vol 287 (23) ◽  
pp. 5218-5235 ◽  
Author(s):  
Xiaofeng Li ◽  
Jiapo Wang ◽  
Weimin Wu ◽  
Hao Gao ◽  
Na Liu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Suppressor Cells ◽  
Signalling Pathway ◽  
Myeloid Derived Suppressor Cells ◽  
Epithelial Ovarian Cancer Cell ◽  
Stat3 Signalling

STAT3 signalling pathway is involved in the activation of microglia induced by 2.45 GHz electromagnetic fields

2010 ◽  
Vol 86 (1) ◽  
pp. 27-36 ◽  
Author(s):  
Yutong Hao ◽  
Xuesen Yang ◽  
Chunhai Chen ◽  
Yuan-Wang ◽  
Xubu Wang ◽  
...  
Keyword(s):  
Electromagnetic Fields ◽  
Signalling Pathway ◽  
Stat3 Signalling

scholarly journals Therapeutic Effect of HGF on NASH Mice Through HGF/c-Met and JAK2-STAT3 Signalling Pathway

2018 ◽  
Vol 17 (3) ◽  
pp. 501-510 ◽  
Author(s):  
Ning Li ◽  
Zhangfeng Dou ◽  
Jinchun Liu ◽  
Bao Chai ◽  
Yue Li ◽  
...  
Keyword(s):  
Therapeutic Effect ◽  
Signalling Pathway ◽  
Stat3 Signalling

Lactobacillus fermentum IM12 attenuates inflammation in mice by inhibiting NF-κB-STAT3 signalling pathway

2017 ◽  
Vol 8 (3) ◽  
pp. 407-419 ◽  
Author(s):  
S.-M. Lim ◽  
H.M. Jang ◽  
S.-E. Jang ◽  
M.J. Han ◽  
D.-H. Kim
Keyword(s):  
Peritoneal Macrophages ◽  
Signalling Pathway ◽  
Lactobacillus Fermentum ◽  
Trinitrobenzene Sulfonic Acid ◽  
Myeloperoxidase Activity ◽  
Paw Oedema ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Stat3 Signalling ◽  
Inflammatory Effect

In the present study, we isolated Lactobacillus fermentum IM12 from human gut microbiota, which strongly inhibited interleukin (IL)-6 expression and STAT3 activation in lipopolysaccharide (LPS)-stimulated murine peritoneal macrophages, and examined its anti-inflammatory effect in mice with carrageenan-induced hind-paw oedema (CIE) or 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis (TIC). Oral administration of IM12 (0.2×109, 1×109 or 5×109 cfu/mouse, once a day for 3 days) in mice with CIE significantly suppressed the increase of oedema volume and thickness, as well as myeloperoxidase activity and IL-6, IL-17, NO, and prostaglandin E2 levels in the carrageenan-stimulated paw. Treatment with IM12 (1×109 cfu/mouse, once a day for 3 days) in mice with TIC significantly suppressed colon shortening, and myeloperoxidase activity and IL-6 and IL-17 levels. Treatment with IM12 in mice with CIE or TIC also suppressed the expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2, as well as activation of nuclear factor kappa beta (NF-κB) and signal transducer and activator of transcription 3 (STAT3). Furthermore, IM12 significantly inhibited the expression of iNOS, and COX-2, as well as activation of NF-κB in LPS-stimulated mouse peritoneal macrophages. The inflammatory effect of heat-inactivated IM12 was significantly different to that of live IM12 in mice with TIC, although anti-inflammatory effect of IM12 was reduced by heat treatment. Based on these findings, IM12 may attenuate inflammation by inhibiting NF-κB-STAT3 signalling pathway.

STAT3 mutations correlated with hyper-IgE syndrome lead to blockage of IL-6/STAT3 signalling pathway

2012 ◽  
Vol 37 (2) ◽  
pp. 243-257 ◽  
Author(s):  
Jianxin He ◽  
Jie Shi ◽  
Ximing Xu ◽  
Wenhua Zhang ◽  
Yuxin Wang ◽  
...  
Keyword(s):  
Signalling Pathway ◽  
Hyper Ige Syndrome ◽  
Stat3 Signalling ◽  
Stat3 Mutations

scholarly journals Novel role of STAT3 in microglia-dependent neuroinflammation after experimental subarachnoid haemorrhage

2021 ◽  
pp. svn-2021-001028
Author(s):  
Zhiyuan Vera Zheng ◽  
Junfan Chen ◽  
Hao Lyu ◽  
Sin Yu Erica Lam ◽  
Gang Lu ◽  
...  
Keyword(s):  
Subarachnoid Haemorrhage ◽  
Inflammatory Responses ◽  
Morphological Changes ◽  
Neuronal Loss ◽  
Signalling Pathway ◽  
Janus Kinase ◽  
Signal Transducer ◽  
Experimental Subarachnoid Haemorrhage ◽  
Stat3 Signalling

Background and purposeSignal transducer and activator of transcription 3 (STAT3) may contribute to the proinflammation in the central nervous system diseases by modulating the microglial responses. Thus, this study was intended to investigate the effect of STAT3 on microglia-dependent neuroinflammation and functional outcome after experimental subarachnoid haemorrhage (SAH).MethodsThe SAH model was established by endovascular perforation in the mouse. Real-time PCR (RtPCR) and western blot were used to examine the dynamic STAT3 signalling pathway responses after SAH. To clarify the role of the STAT3 signalling pathway in the microglia-dependent neuroinflammation after SAH, the microglia-specific STAT3 knockout (KO) mice were generated by the Cre-LoxP system. The neurological functions were assessed by Catwalk and Morris water maze tests. Neuronal loss after SAH was determined by immunohistochemistry staining. Microglial polarisation status after STAT3 KO was then examined by RtPCR and immunofluorescence.ResultsThe STAT3 and Janus kinase-signal transducer 2 activated immediately with the upregulation and phosphorylation after SAH. Downstream factors and related mediators altered dynamically and accordingly. Microglial STAT3 deletion ameliorated the neurological impairment and alleviated the early neuronal loss after SAH. To investigate the underlying mechanism, we examined the microglial reaction after STAT3 KO. STAT3 deletion reversed the increase of microglia after SAH. Loss of STAT3 triggered the early morphological changes of microglia and primed microglia from M1 to M2 polarisation. Functionally, microglial STAT3 deletion suppressed the SAH-induced proinflammation and promoted the anti-inflammation in the early phase.ConclusionsSTAT3 is closely related to the microglial polarisation transition and modulation of microglia-dependent neuroinflammation. Microglial STAT3 deletion improved neurological function and neuronal survival probably through promoting M2 polarisation and anti-inflammatory responses after SAH. STAT3 may serve as a promising therapeutic target to alleviate early brain injury after SAH.

scholarly journals Inhibition of STAT3 enhances sensitivity to tamoxifen in tamoxifen-resistant breast cancer cells

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Seo Yun Moon ◽  
Heejin Lee ◽  
Seoree Kim ◽  
Ji Hyung Hong ◽  
Sang Hoon Chun ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Expression ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Signalling Pathway ◽  
Expression Levels ◽  
Er Positive ◽  
Tamoxifen Resistant ◽  
Stat3 Signalling ◽  
Mcf 7

Abstract Background The mechanisms of endocrine resistance are complex, and deregulation of several oncogenic signalling pathways has been proposed. We aimed to investigate the role of the EGFR and Src-mediated STAT3 signalling pathway in tamoxifen-resistant breast cancer cells. Methods The ER-positive luminal breast cancer cell lines, MCF-7 and T47D, were used. We have established an MCF-7-derived tamoxifen-resistant cell line (TamR) by long-term culture of MCF-7 cells with 4-hydroxytamoxifen. Cell viability was determined using an MTT assay, and protein expression levels were determined using western blot. Cell cycle and annexin V staining were analysed using flow cytometry. Results TamR cells showed decreased expression of estrogen receptor and increased expression of EGFR. TamR cells showed an acceleration of the G1 to S phase transition. The protein expression levels of phosphorylated Src, EGFR (Y845), and STAT3 was increased in TamR cells, while phosphorylated Akt was decreased. The expression of p-STAT3 was enhanced according to exposure time of tamoxifen in T47D cells, suggesting that activation of STAT3 can cause tamoxifen resistance in ER-positive breast cancer cells. Both dasatinib (Src inhibitor) and stattic (STAT3 inhibitor) inhibited cell proliferation and induced apoptosis in TamR cells. However, stattic showed a much stronger effect than dasatinib. Knockdown of STAT3 expression by siRNA had no effect on sensitivity to tamoxifen in MCF-7 cells, while that enhanced sensitivity to tamoxifen in TamR cells. There was not a significant synergistic effect of dasatinib and stattic on cell survival. TamR cells have low nuclear p21(Cip1) expression compared to MCF-7 cells and inhibition of STAT3 increased the expression of nuclear p21(Cip1) in TamR cells. Conclusions The EGFR and Src-mediated STAT3 signalling pathway is activated in TamR cells, and inhibition of STAT3 may be a potential target in tamoxifen-resistant breast cancer. An increase in nuclear p21(Cip1) may be a key step in STAT3 inhibitor-induced cell death in TamR cells.

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