scholarly journals Systems Pharmacogenomics Finds RUNX1 Is an Aspirin-Responsive Transcription Factor Linked to Cardiovascular Disease and Colon Cancer

EBioMedicine ◽  
2016 ◽  
Vol 11 ◽  
pp. 157-164 ◽  
Author(s):  
Deepak Voora ◽  
A. Koneti Rao ◽  
Gauthami S. Jalagadugula ◽  
Rachel Myers ◽  
Emily Harris ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Colon Cancer ◽  
Transcription Factor

scholarly journals Transgelin interacts with PARP1 and affects Rho signaling pathway in human colon cancer cells

2020 ◽  
Author(s):  
Zhen-xian Lew ◽  
Hui-min Zhou ◽  
Yuan-yuan Fang ◽  
Zhen Ye ◽  
Wa Zhong ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Colon Cancer ◽  
Transcription Factor ◽  
High Performance Liquid Chromatography ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
High Performance ◽  
Colon Cancer Cells ◽  
Over Expression ◽  
Key Genes

Abstract Background: Transgelin, an actin-binding protein, is associated with the cytoskeleton remodeling. Our previous studies found that transgelin was up-regulated in node-positive colorectal cancer versus in node-negative disease. Over-expression of TAGLN affected the expression of 256 downstream transcripts and increased the metastatic potential of colon cancer cells in vitro and in vivo. This study aims to explore the mechanisms that transgelin participates in the metastasis of colon cancer cells.Methods: Immunofluorescence and immunoblotting analysis were used to determine the cellular localization of the endogenous and exogenous transgelin in colon cancer cells. Co-immunoprecipitation and subsequent high performance liquid chromatography/tandem mass spectrometry were performed to identify the proteins potentially interacting with transgelin. Bioinformatics methods were used to analyze the 256 downstream transcripts regulated by transgelin to discriminate the specific key genes and signaling pathways. By analyzing the promoter region of these key genes, GCBI tools were used to predict the potential transcription factor(s) for these genes. The predicted transcription factors were matching to the proteins that have been identified to potentially interact with transgelin. The interaction between transgelin and these transcription factors was verified by co-immunoprecipitation and immunoblotting.Results: Transgelin was found to localize both in the cytoplasm and the nucleus of colon cancer cells. 297 proteins have been identified to interact with transgelin by co-immunoprecipitation and subsequent high performance liquid chromatography/mass spectrometry. Over-expression of TAGLN could lead to differential expression of 184 downstream genes. By constructing the network of gene-encoded proteins, 7 genes (CALM1, MYO1F, NCKIPSD, PLK4, RAC1, WAS and WIPF1) have been discriminated as key genes using network topology analysis. They are mostly involved in the Rho signaling pathway. Poly ADP-ribose polymerase-1 (PARP1) was predicted as the unique transcription factor for the key genes and concurrently matching to the DNA-binding proteins potentially interacting with transgelin. Immunoprecipitation validated that PARP1 interacted with transgelin in human RKO colon cancer cells.Conclusions: The results of this study suggest that transgelin binds to PARP1 and regulates the expression of the downstream key genes mainly involving Rho signaling pathway, thus participates in the metastasis of colon cancer.

scholarly journals Peroxiporins Are Induced Upon Oxidative Stress Insult and Are Associated with Oxidative Stress Resistance in Colon Cancer Cell Lines

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1856
Author(s):  
Ana Čipak Gašparović ◽  
Lidija Milković ◽  
Claudia Rodrigues ◽  
Monika Mlinarić ◽  
Graça Soveral
Keyword(s):  
Oxidative Stress ◽  
Colon Cancer ◽  
Transcription Factor ◽  
Cell Lines ◽  
Stress Resistance ◽  
Therapy Resistance ◽  
Colon Cancer Cell ◽  
Colon Cancer Cell Lines ◽  
Intracellular Ros ◽  
Ht 29

Oxidative stress can induce genetic instability and change cellular processes, resulting in colorectal cancer. Additionally, adaptation of oxidative defense causes therapy resistance, a major obstacle in successful cancer treatment. Peroxiporins are aquaporin membrane channels that facilitate H2O2 membrane permeation, crucial for regulating cell proliferation and antioxidative defense. Here, we investigated four colon cancer cell lines (Caco-2, HT-29, SW620, and HCT 116) for their sensitivity to H2O2, cellular antioxidative status, and ROS intracellular accumulation after H2O2 treatment. The expression of peroxiporins AQP1, AQP3, and AQP5 and levels of NRF2, the antioxidant transcription factor, and PPARγ, a transcription factor that regulates lipid metabolism, were evaluated before and after oxidative insult. Of the four tested cell lines, HT-29 was the most resistant and showed the highest expression of all tested peroxiporins and the lowest levels of intracellular ROS, without differences in GSH levels, catalase activity, nor NF2 and PPARγ levels. Caco-2 shows high expression of AQP3 and similar resistance as HT-29. These results imply that oxidative stress resistance can be obtained by several mechanisms other than the antioxidant defense system. Regulation of intracellular ROS through modulation of peroxiporin expression may represent an additional strategy to target the therapy resistance of cancer cells.

scholarly journals Nuclear Transcription Factor Kappa B (NF-кB) and Molecular Damage Mechanisms in Acute Cardiovascular Diseases. A Review

2018 ◽  
Vol 4 (2) ◽  
pp. 65-72 ◽  
Author(s):  
Roxana Buzas ◽  
Alexandru Florin Rogobete ◽  
Sonia Elena Popovici ◽  
Tudor Mateescu ◽  
Teodora Hoinoiu ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Transcription Factor ◽  
Cardiovascular Diseases ◽  
Molecular Mechanisms ◽  
Severe Form ◽  
Molecular Therapy ◽  
Atheromatous Plaque ◽  
Early Evaluation ◽  
Nuclear Transcription Factor ◽  
Molecular Damage

Abstract Worldwide, cardiovascular diseases (CVDs) represent one of the main causes of morbidity and mortality, and acute coronary syndromes are responsible for a large number of sudden cardiac deaths. One of the main challenges that still exist in this area is represented by the early detection and targeted monitoring of the pathophysiology involved in CVDs. During the last couple of years, researchers have highlighted the importance of molecular and epigenetic mechanisms involved in the initiation and augmentation of CVDs, culminating in their most severe form represented by acute myocardial infarction. One of the most studied molecular factors involved in this type of pathology is represented by nuclear transcription factor kappa B (NF-κB), as well as the involvement of microRNAs (miRNAs). It has been suggested that miRNAs can also be involved in the complex process of atheromatous plaque vulnerabilization that leads to an acute cardiac event. In this review paper, we describe the most important molecular mechanisms involved in the pathogenesis of CVDs and atheromatous plaque progression and vulnerabilization, which include molecular mechanisms dependent on NF-κB. For this paper, we used international databases (PubMed and Scopus). The keywords used for the search were “miRNAs biomarkers”, “miRNAs in cardiovascular disease”, “NF-κB in cardiovascular disease”, “molecular mechanism in cardiovascular disease”, and “myocardial NF-κB mechanisms”. Numerous molecular reactions that have NF-κB as a trigger are involved in the pathogenesis of CVDs. Moreover, miRNAs play an important role in initiating and aggravating certain segments of CVDs. Therefore, miRNAs can be used as biomarkers for early evaluation of CVDs. Furthermore, in the future, miRNAs could be used as a targeted molecular therapy in order to block certain mechanisms responsible for inducing CVDs and leading to acute cardiovascular events.

scholarly journals MicroRNA-transcription factor interactions and their combined effect on target gene expression in colon cancer cases

2017 ◽  
Vol 57 (4) ◽  
pp. 192-202 ◽  
Author(s):  
Lila E. Mullany ◽  
Jennifer S. Herrick ◽  
Roger K. Wolff ◽  
John R. Stevens ◽  
Wade Samowitz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
Transcription Factor ◽  
Target Gene ◽  
Combined Effect ◽  
Target Gene Expression ◽  
Factor Interactions

Activating transcription factor 3 promotes colon cancer metastasis

Tumor Biology ◽  
2014 ◽  
Vol 35 (8) ◽  
pp. 8329-8334 ◽  
Author(s):  
Zhi-Yong Wu ◽  
Zheng-mao Wei ◽  
Sheng-Jie Sun ◽  
Jing Yuan ◽  
Shun-Chang Jiao
Keyword(s):  
Colon Cancer ◽  
Transcription Factor ◽  
Cancer Metastasis ◽  
Activating Transcription Factor 3 ◽  
Colon Cancer Metastasis ◽  
Activating Transcription Factor ◽  
Transcription Factor 3
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