scholarly journals Leptin induces the apoptosis of chondrocytes in an in vitro model of osteoarthritis via the JAK2-STAT3 signaling pathway

2016 ◽  
Vol 13 (4) ◽  
pp. 3684-3690 ◽  
Author(s):  
ZI MING ZHANG ◽  
CHAO SHEN ◽  
HAI LI ◽  
QING FAN ◽  
JING DING ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
In Vitro Model ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Vitro Model

scholarly journals MicroRNA-1297 suppressed the Akt/GSK3β signaling pathway and stimulated neural apoptosis in an in vivo sevoflurane exposure model

2021 ◽  
Vol 49 (4) ◽  
pp. 030006052098210
Author(s):  
Quan Wang ◽  
Jingcong Luo ◽  
Ruiqiang Sun ◽  
Jia Liu
Keyword(s):  
Protein Expression ◽  
Signaling Pathway ◽  
Neuronal Apoptosis ◽  
In Vitro Model ◽  
Nervous System Development ◽  
Exposure Model ◽  
Control Group ◽  
Pten Protein ◽  
Vitro Model

Objective Common inhalation anesthetics used for clinical anesthesia (such as sevoflurane) may induce nerve cell apoptosis during central nervous system development. Furthermore, anesthetics can produce cognitive impairments, such as learning and memory impairments, that continue into adulthood. However, the precise mechanism remains largely undefined. We aimed to determine the function of microRNA-1297 (miR-1297) in sevoflurane-induced neurotoxicity. Methods Reverse transcription-polymerase chain reaction assays were used to analyze miR-1297 expression in sevoflurane-exposed mice. MTT and lactate dehydrogenase (LDH) assays were used to measure cell growth, and neuronal apoptosis was analyzed using flow cytometry. Western blot analyses were used to measure PTEN, PI3K, Akt, and GSK3β protein expression. Results In sevoflurane-exposed mice, miR-1297 expression was up-regulated compared with the control group. MiR-1297 up-regulation led to neuronal apoptosis, inhibition of cell proliferation, and increased LDH activity in the in vitro model of sevoflurane exposure. MiR-1297 up-regulation also suppressed the Akt/GSK3β signaling pathway and induced PTEN protein expression in the in vitro model. PTEN inhibition (VO-Ohpic trihydrate) reduced PTEN protein expression and decreased the effects of miR-1297 down-regulation on neuronal apoptosis in the in vitro model. Conclusion Collectively, the results indicated that miR-1297 stimulates sevoflurane-induced neurotoxicity via the Akt/GSK3β signaling pathway by regulating PTEN expression.

A natural product phillygenin suppresses osteosarcoma growth and metastasis by regulating the SHP-1/JAK2/STAT3 signaling

2021 ◽  
Vol 85 (2) ◽  
pp. 307-314
Author(s):  
Xiaomin Ding ◽  
Danqing Lu ◽  
Jianbo Fan
Keyword(s):  
Cell Growth ◽  
Signaling Pathway ◽  
Janus Kinase ◽  
Potential Candidate ◽  
Osteosarcoma Cell ◽  
Cancer Cell Growth ◽  
Functional Roles ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

ABSTRACT Osteosarcoma represents one of the most devastating cancers due to its high metastatic potency and fatality. Osteosarcoma is insensitive to traditional chemotherapy. Identification of a small molecule that blocks osteosarcoma progression has been a challenge in drug development. Phillygenin, a plant-derived tetrahydrofurofuran lignin, has shown to suppress cancer cell growth and inflammatory response. However, how phillygenin plays functional roles in osteosarcoma has remained unveiled. In this study, we showed that phillygenin inhibited osteosarcoma cell growth and motility in vitro. Further mechanistic studies indicated that phillygenin blocked STAT3 signaling pathway. Phillygenin led to significant downregulation of Janus kinase 2 and upregulation of Src homology region 2 domain-containing phosphatase 1. Gene products of STAT3 regulating cell survival and invasion were also inhibited by phillygenin. Therefore, our studies provided the first evidence that phillygenin repressed osteosarcoma progression by interfering STAT3 signaling pathway. Phillygenin is a potential candidate in osteosarcoma therapy.

β-Asarone Inhibits Neuronal Apoptosis via the CaMKII/CREB/Bcl-2 Signaling Pathway in an in vitro Model and AβPP/PS1 Mice

2013 ◽  
Vol 33 (3) ◽  
pp. 863-880 ◽  
Author(s):  
Gang Wei ◽  
Yun-bo Chen ◽  
Dong-Feng Chen ◽  
Xiao-Ping Lai ◽  
Dong-Hui Liu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Neuronal Apoptosis ◽  
In Vitro Model ◽  
Vitro Model

scholarly journals Dynasore suppresses cell proliferation, migration, and invasion and enhances the antitumor capacity of cisplatin via STAT3 pathway in osteosarcoma

2019 ◽  
Vol 10 (10) ◽  
Author(s):  
Binlong Zhong ◽  
Deyao Shi ◽  
Fashuai Wu ◽  
Shangyu Wang ◽  
Hongzhi Hu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Mapk Pathway ◽  
Migration And Invasion ◽  
G1 Arrest ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Candidate Drug

Abstract Osteosarcoma (OS) is the most common malignant bone tumor. The prognosis of metastatic and recurrent OS patients still remains unsatisfactory. Cisplatin reveals undeniable anti-tumor effect while induces severe side effects that threatening patients’ health. Dynasore, a cell-permeable small molecule that inhibits dynamin activity, has been widely studied in endocytosis and phagocytosis. However, the anti-tumor effect of dynasore on OS has not yet been ascertained. In the present study, we suggested that dynasore inhibited cell proliferation, migration, invasion, and induced G0/G1 arrest of OS cells. Besides, dynasore repressed tumorigenesis of OS in xenograft mouse model. In addition, we demonstrated that dynasore improved the anti-tumor effect of cisplatin in vitro and in vivo without inducing nephrotoxicity and hepatotoxicity. Mechanistically, dynasore repressed the expression of CCND1, CDK4, p-Rb, and MMP-2. Furthermore, we found that dynasore exerts anti-tumor effects in OS partially via inhibiting STAT3 signaling pathway but not ERK-MAPK, PI3K-Akt or SAPK/JNK pathways. P38 MAPK pathway served as a negative regulatory mechanism in dynasore induced anti-OS effects. Taken together, our study indicated that dynasore does suppress cell proliferation, migration, and invasion via STAT3 signaling pathway, and enhances the antitumor capacity of cisplatin in OS. Our results suggest that dynasore is a novel candidate drug to inhibit the tumor growth of OS and enhance the anti-tumor effects of cisplatin.

JAK2-STAT3 signaling pathway mediates thrombin-induced proinflammatory actions of microglia in vitro☆

2008 ◽  
Vol 204 (1-2) ◽  
pp. 118-125 ◽  
Author(s):  
C HUANG ◽  
R MA ◽  
S SUN ◽  
G WEI ◽  
Y FANG ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

scholarly journals Escin Sodium Improves the Prognosis of Acute Pancreatitis via Promoting Cell Apoptosis by Suppression of the ERK/STAT3 Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-26
Author(s):  
Qian Zhang ◽  
Chen Zhao ◽  
Lei Zhang ◽  
Kai Sun ◽  
Linlin Yu ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Inflammatory Responses ◽  
Horse Chestnut ◽  
Inflammatory Disorder ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

Acute pancreatitis (AP), an inflammatory disorder of the pancreas, can cause systemic inflammatory responses. Escin Sodium (ES), a natural mixture of triterpene saponins extracted from the dry ripe fruit of Fructus Aesculi or horse chestnut crude, has been demonstrated to have antiedematous, anti-inflammatory, and antiexudative effects. We here aim to investigate the effects of ES pretreatment on AP in vivo and in vitro and explore its potential molecular mechanism. In the present study, we demonstrated that ES pretreatment could apparently decrease amylase and lipase, downregulate inflammatory cytokines, and attenuate pancreatic damage. Additionally, the increased expression of apoptotic-related proteins and the results of flow cytometry demonstrated the effects of ES on promoting apoptosis in acinar cells. Moreover, ES could enhance mitochondrial membrane potential (MMP, ΔΨm) and reactive oxygen species (ROS) level and reduce intracellular calcium concentration, which are closely related to mitochondrial-mediated death. The effect of ES pretreatment on acinar cell apoptosis was furtherly confirmed by the regulatory pathway of the ERK/STAT3 axis. These results suggest that ES attenuates the severity of AP by enhancing cell apoptosis via suppressing the ERK/STAT3 signaling pathway. These findings provide evidence for ES which is treated as a novel and potent therapeutic for the treatment of AP.

scholarly journals Bufalin suppresses tumour microenvironment-mediated angiogenesis by inhibiting the STAT3 signaling pathway

2021 ◽  
Author(s):  
Ke Xu ◽  
Kai Fang ◽  
Yueping Zhan ◽  
Yuqian Wang ◽  
Chengqi Wu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Endothelial Cells ◽  
Tumor Microenvironment ◽  
Signaling Pathway ◽  
Umbilical Vein ◽  
Tumour Microenvironment ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

Abstract Background Anti-angiogenesis therapy has increasingly become an important strategy for the treatment of colorectal cancer. Recent studies have shown that tumor microenvironment (TME) promotes tumour angiogenesis. Bufalin is an active compound whose anti-tumor efficacy has been proven by previous studies. However, there are very few studies on the anti-angiogenic effects of bufalin. Methods Herein, human umbilical vein endothelial cells (HUVEC) tube formation, migration and adhesion test were used to assess angiogenesis in vitro. Western blot and quantitative PCR were used to detect relevant protein levels and the expressions of mRNAs. Subcutaneous xenograft tumor model and hepatic metastasis model in mice were established to investigate the influence of bufalin on angiogenesis-mediated by TME in vivo. Results We found that the angiogenesis mediated by tumor microenvironment cells was significantly inhibited in the present of bufalin. The results demonstrated that the pro-angiogenic gene in HUVEC such as VEGF, PDGFA, E-selectin and P-selectin were downregulated by bufalin, and the downregulation was regulated by inhibiting the STAT3 pathway. Overexpression STAT3 could reverse the inhibitory effect of bufalin on angiogenesis. What is more, few reduction of angiogenesis when bufalin directly acted on tumor microenvironment cells. Conclusion Our findings demonstrate that bufalin suppresses tumour microenvironment-mediated angiogenesis by inhibiting the STAT3 signaling pathway of vascular endothelial cells, which reveals that bufalin may be used as a new anti-angiogenic adjuvant therapy medicine in the treatment of colorectal cancer.

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