Melittin Suppresses VEGF-A-Induced Tumor Growth by Blocking VEGFR-2 and the COX-2-Mediated MAPK Signaling Pathway

2012 ◽  
Vol 75 (11) ◽  
pp. 1922-1929 ◽  
Author(s):  
Jeong-Eun Huh ◽  
Jung Won Kang ◽  
Dongwoo Nam ◽  
Yong-Hyeon Baek ◽  
Do-Young Choi ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Cox 2

scholarly journals 18α-Glycyrrhetinic acid monoglucuronide as an anti-inflammatory agent through suppression of the NF-κB and MAPK signaling pathway

MedChemComm ◽  
2017 ◽  
Vol 8 (7) ◽  
pp. 1498-1504 ◽  
Author(s):  
Bo Li ◽  
Yongan Yang ◽  
Liuzeng Chen ◽  
Shichao Chen ◽  
Jing Zhang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Glycyrrhetinic Acid ◽  
Inflammatory Activity ◽  
Inflammatory Agent ◽  
Cox 2 ◽  
Anti Inflammatory

18α-GAMG exhibited strong anti-inflammatory activity through inhibiting the expression of iNOS, COX-2, and MAPKs, as well as activation of NF-κB.

MicroRNA‐329‐mediated PTTG1 downregulation inactivates the MAPK signaling pathway to suppress cell proliferation and tumor growth in cholangiocarcinoma

2018 ◽  
Vol 120 (6) ◽  
pp. 9964-9978 ◽  
Author(s):  
Zhi‐Gao Hu ◽  
Chao‐Wen Zheng ◽  
Hui‐Zhao Su ◽  
Yong‐Lian Zeng ◽  
Cheng‐Jie Lin ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Growth ◽  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Suppress Cell Proliferation

scholarly journals Elevated microRNA-145 inhibits the development of oral squamous cell carcinoma through inactivating ERK/MAPK signaling pathway by down-regulating HOXA1

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Junhai Ding ◽  
Dubin Sun ◽  
Pengfeng Xie
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Erk Mapk

AbstractBackground: Oral cancer is one of the most frequent solid cancers worldwide, and oral squamous cell carcinoma (OSCC) constitutes approximately 90% of oral cancers. The discovery of reliable prognostic indicators would be a potential strategy for OSCC treatment. In the present study, we aim to explore the underlying mechanism by which microRNA-145 (miR-145) affected OSCC. Methods: Forty-eight patients diagnosed with OSCC were enrolled to obtain the OSCC tissues and adjacent normal tissues. The targeting relationship between miR-145 and Homeobox A1 (HOXA1) was verified. In order to assess the effects of miR-145 in OSCC and the detailed regulatory mechanism, the SCC-9 cell line was adopted, in which expression of miR-145 and HOXA1 were altered by transfection. Then, a series of in vitro and in vivo experiments were performed to evaluate the cell viability, migration, invasion, and tumor growth. Results: miR-145 was poorly expressed and HOXA1 was highly expressed in OSCC. HOXA1 was verified as a target of miR-145 to mediate the activation of the extracellular signal-regulated kinase/mitogen activated protein kinase (ERK/MAPK) signaling pathway. In the circumstance of miR-145 elevation or HOXA1 depletion, the SCC-9 cell line manifested with inhibited cell viability, invasion, and migration in vitro, coupled with reduced tumor growth in vivo, with a decreased expression of ERK/MAPK signaling pathway-related genes/proteins. Conclusion: These findings suggested that miR-145 can inhibit HOXA1 to inactivate the ERK/MAPK signaling pathway, thereby suppressing OSCC cell proliferation, migration, and invasion to further inhibit the development of OSCC, highlighting a novel therapeutic target for the OSCC treatment.

scholarly journals Cholesterol Enhances Colorectal Cancer Progression via ROS Elevation and MAPK Signaling Pathway Activation

2017 ◽  
Vol 42 (2) ◽  
pp. 729-742 ◽  
Author(s):  
Caihua Wang ◽  
Peiwei Li ◽  
Junmei Xuan ◽  
Chunpeng Zhu ◽  
Jingjing Liu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
Signaling Pathway ◽  
High Fat Diet ◽  
Ldl Receptor ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
High Fat

Background/Aims: Elevated serum cholesterol levels were linked to a higher risk of colorectal adenoma and colorectal cancer (CRC), while the effect of cholesterol on CRC metastasis has not been widely studied. Methods: CRC patients were enrolled to evaluate the association between low-density lipoprotein cholesterol (LDL) and CRC metastases, and LDL receptor (LDLR) level of the CRC tissue was assessed by immunohistochemistry. The effects of LDL on cell proliferation, migration and stemness were assessed in CRC cells in vitro, and the effects of high fat diet (HFD) on tumor growth and intestinal tumorigenicity were investigated in vivo. ROS assays, gene expression array analysis and western blot were used to explore the mechanisms of LDL in CRC progression. Results: The level of LDL was positively correlated with liver metastases, and a higher level of LDL receptor (LDLR) expression was associated with advanced N and M stages of CRC. In vitro, LDL promoted the migration and sphere formation of CRC cells and induced upregulated expression of “stemness” genes including Sox2, Oct4, Nanog and Bmi 1. High-fat diet (HFD) significantly enhanced tumor growth in vivo, and was associated with a shorter intestinal length in azoxymethane/dextran sodium sulfate (AOM/DSS)-treated mice. Furthermore, LDL significantly elevated reactive oxygen species (ROS) levels and Whole Human Genome Microarray found 87 differentially expressed genes between LDL-treated CRC cells and controls, which were largely clustered in the MAP kinase (MAPK) signaling pathway. Conclusions: LDL enhances intestinal inflammation and CRC progression via activation of ROS and signaling pathways including the MAPK pathway. Inflammation is strongly associated with cancer initiation, and the role of LDL in intestinal tumorigenicity should be further explored.

scholarly journals Nuclear Export Protein CSE1L Interacts with P65 and Promotes NSCLC Growth via NF-κB/MAPK Pathway

2020 ◽  
Author(s):  
Hechun lin ◽  
Jing Li ◽  
Dongdong Chen ◽  
Xiao Zhang ◽  
Tao Yu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tumor Growth ◽  
Signaling Pathway ◽  
Nuclear Export ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Clinical Samples ◽  
Rna Seq ◽  
Survival Times

Abstract Background: Cancer cells can utilize the transportins into and out of the nucleus to stimulate tumor growth and to effectively evade apoptotic mechanisms. We aimed to identify transportins that are overexpressed in Non-small cell lung cancer (NSCLC) and might be targeted to slow the tumor growth. Methods: Using the ONCOMINE and Gene Expression Omnibus (GEO) databases, we compared the gene expression of 24 importins and exportins in 20 cancer microarray datasets and then analyzed the survival of the candidate genes, CSE1L (Chromosome Segregation Like 1 protein/CAS) was finally selected. The expression level of CSE1L was detected in both NSCLC cells and clinical samples. To evaluate the function of CSE1L in vitro and in vivo, CCK-8, colony formation, cell apoptosis and subcutaneous tumor model were performed. The co-immunoprecipitation experiment combined with mass spectrometry was conducted to find out the protein interacted with CSE1L. The underlying mechanism was investigated by RNA-seq and Western blot.Results: 7 transportins were over-expressed in NSCLC patients, and higher expression of CSE1L and XPO5 are associated with shorter survival times. CSE1L was a exportin while the role of tumorigenicity in NSCLC remain unknown. Increased expression of CSE1L in tumor tissues associated with shorter survival times and advanced pathological stage of patients with cancer. The gain- and loss-of-function assays indicated that CSE1L promoted NSCLC cells proliferation and inhibits cells apoptosis. Additionally, we confirmed that CSE1L interacted with RELA (named as P65), and affected its expression in nucleus. RNA-seq results indicated that CSE1L activated the MAPK signaling pathway in NSCLC cells by increasing activity of P65.Conclusions: We reveal the oncogenic role of CSE1L in NSCLC cancer carcinogenesis. CSE1L promotes proliferation of NSCLC cells by activating the MAPK signaling pathway and inhibiting apoptosis in coordination with P65. Our findings highlight that CSE1L may be a target for the treatment of NSCLC cancer.

scholarly journals Attenuation of High Glucose-Induced Damage in RPE Cells through p38 MAPK Signaling Pathway Inhibition

2021 ◽  
Vol 12 ◽  
Author(s):  
Grazia Maugeri ◽  
Claudio Bucolo ◽  
Filippo Drago ◽  
Settimio Rossi ◽  
Michelino Di Rosa ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
P38 Mapk ◽  
High Glucose ◽  
Retinal Pigment ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Rpe Cells ◽  
Cox 2

This study aimed to investigate the high glucose damage on human retinal pigment epithelial (RPE) cells, the role of p38 MAPK signaling pathway and how dimethyl fumarate can regulate that. We carried out in vitro studies on ARPE-19 cells exposed to physiological and high glucose (HG) conditions, to evaluate the effects of DMF on cell viability, apoptosis, and expression of inflammatory and angiogenic biomarkers such as COX-2, iNOS, IL-1β, and VEGF. Our data have demonstrated that DMF treatment attenuated HG-induced apoptosis, as confirmed by reduction of BAX/Bcl-2 ratio. Furthermore, in RPE cells exposed to HG we observed a significant increase of iNOS, COX-2, and IL-1β expression, that was reverted by DMF treatment. Moreover, DMF reduced the VEGF levels elicited by HG, inhibiting p38 MAPK signaling pathway. The present study demonstrated that DMF provides a remarkable protection against high glucose-induced damage in RPE cells through p38 MAPK inhibition and the subsequent down-regulation of VEGF levels, suggesting that DMF is a small molecule that represents a good candidate for diabetic retinopathy treatment and warrants further in vivo and clinical evaluation.

MAPK: A Key Player in the Development and Progression of Stroke

2020 ◽  
Vol 19 (4) ◽  
pp. 248-256
Author(s):  
Yangmin Zheng ◽  
Ziping Han ◽  
Haiping Zhao ◽  
Yumin Luo
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Complex Disease ◽  
Therapeutic Targets ◽  
Cell Types ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Effective Prevention ◽  
Prevention And Treatment ◽  
Different Cell Types

Conclusion: Stroke is a complex disease caused by genetic and environmental factors, and its etiological mechanism has not been fully clarified yet, which brings great challenges to its effective prevention and treatment. MAPK signaling pathway regulates gene expression of eukaryotic cells and basic cellular processes such as cell proliferation, differentiation, migration, metabolism and apoptosis, which are considered as therapeutic targets for many diseases. Up to now, mounting evidence has shown that MAPK signaling pathway is involved in the pathogenesis and development of ischemic stroke. However, the upstream kinase and downstream kinase of MAPK signaling pathway are complex and the influencing factors are numerous, the exact role of MAPK signaling pathway in the pathogenesis of ischemic stroke has not been fully elucidated. MAPK signaling molecules in different cell types in the brain respond variously after stroke injury, therefore, the present review article is committed to summarizing the pathological process of different cell types participating in stroke, discussed the mechanism of MAPK participating in stroke. We further elucidated that MAPK signaling pathway molecules can be used as therapeutic targets for stroke, thus promoting the prevention and treatment of stroke.

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