scholarly journals HER-2/neu over expression in gall bladder adenocarcinoma: A quest for potential therapeutic target

2020 ◽  
Vol 63 (2) ◽  
pp. 214
Author(s):  
Puja Sakhuja ◽  
Pragya Jain ◽  
Surbhi Goyal ◽  
Geeta Chauhan ◽  
Kaushik Majumdar ◽  
...  
Keyword(s):  
Gall Bladder ◽  
Therapeutic Target ◽  
Potential Therapeutic Target ◽  
Over Expression ◽  
Her 2 ◽  
Bladder Adenocarcinoma

scholarly journals Histone Methyltransferase EZH2: A Potential Therapeutic Target for Kidney Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Tingting Li ◽  
Chao Yu ◽  
Shougang Zhuang
Keyword(s):  
Animal Models ◽  
Therapeutic Target ◽  
Renal Fibrosis ◽  
Kidney Diseases ◽  
Disease Model ◽  
Kidney Injury ◽  
Potential Therapeutic Target ◽  
Over Expression ◽  
Ezh2 Expression

Enhancer of zeste homolog 2 (EZH2) is a histone-lysine N-methyltransferase enzyme that catalyzes the addition of methyl groups to histone H3 at lysine 27, leading to gene silencing. Mutation or over-expression of EZH2 has been linked to many cancers including renal carcinoma. Recent studies have shown that EZH2 expression and activity are also increased in several animal models of kidney injury, such as acute kidney injury (AKI), renal fibrosis, diabetic nephropathy, lupus nephritis (LN), and renal transplantation rejection. The pharmacological and/or genetic inhibition of EZH2 can alleviate AKI, renal fibrosis, and LN, but potentiate podocyte injury in animal models, suggesting that the functional role of EZH2 varies with renal cell type and disease model. In this article, we summarize the role of EZH2 in the pathology of renal injury and relevant mechanisms and highlight EZH2 as a potential therapeutic target for kidney diseases.

scholarly journals miR-518a-3p Suppresses Triple-Negative Breast Cancer Invasion and Migration Through Regulation of TMEM2

2020 ◽  
Vol 19 ◽  
pp. 153303382097752
Author(s):  
Lin Gan ◽  
Huachao Yang ◽  
Zhifeng Xiong ◽  
Zailiang Yang ◽  
Ting Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Cell Invasion ◽  
Therapeutic Target ◽  
Triple Negative ◽  
Janus Kinase ◽  
Potential Therapeutic Target ◽  
Invasion And Migration ◽  
Over Expression ◽  
And Migration

MicroRNAs (miRNAs) are emerging as critical mediators in tumors, including triple-negative breast cancer (TNBC). The role of miR-518a-3p in TNBC was investigated to identify potential therapeutic target. Data from KM Plotter database ( www.kmplot.com ) showed that high miR-518a-3p expression was significantly associated with overall survival of patients with TNBC ( p = 0.04). The expression of miR-518a-3p was dysregulated in TNBC cells. Functional assays revealed that over-expression of miR-518a-3p inhibited cell invasion and migration of TNBC. Additionally, miR-518a-3p could target TMEM2 (transmembrane protein 2), and decreased protein and mRNA expression of TMEM2 in TNBC cells. Knockdown of TMEM2 suppressed cell invasion and migration through inhibiting phospho (p)-JAK1 (Janus kinase 1) and p-STAT (signal transducer and activator of transcription protein) 1/2. Moreover, over-expression of TMEM2 counteracted the suppressive effect of miR-518a-3p on TNBC invasion and migration through promoting the levels of p-JAK1 and p-STAT1/2. In conclusion, miR-518a-3p negatively regulates the JAK/STAT pathway via targeting TMEM2 and suppresses invasion and migration in TNBC, suggesting that miR-518a-3p may be a potential therapeutic target in TNBC.

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