scholarly journals MicroRNA Networks Modulate Oxidative Stress in Cancer

2019 ◽  
Vol 20 (18) ◽  
pp. 4497 ◽  
Author(s):  
Yang-Hsiang Lin
Keyword(s):  
Oxidative Stress ◽  
Tumor Suppressors ◽  
Target Gene ◽  
Neurological Diseases ◽  
Rna Molecules ◽  
Functional Roles ◽  
Cancer Hallmarks ◽  
Small Ncrnas ◽  
Essential Properties ◽  
Microrna Networks

Imbalanced regulation of reactive oxygen species (ROS) and antioxidant factors in cells is known as “oxidative stress (OS)”. OS regulates key cellular physiological responses through signal transduction, transcription factors and noncoding RNAs (ncRNAs). Increasing evidence indicates that continued OS can cause chronic inflammation, which in turn contributes to cardiovascular and neurological diseases and cancer development. MicroRNAs (miRNAs) are small ncRNAs that produce functional 18-25-nucleotide RNA molecules that play critical roles in the regulation of target gene expression by binding to complementary regions of the mRNA and regulating mRNA degradation or inhibiting translation. Furthermore, miRNAs function as either tumor suppressors or oncogenes in cancer. Dysregulated miRNAs reportedly modulate cancer hallmarks such as metastasis, angiogenesis, apoptosis and tumor growth. Notably, miRNAs are involved in ROS production or ROS-mediated function. Accordingly, investigating the interaction between ROS and miRNAs has become an important endeavor that is expected to aid in the development of effective treatment/prevention strategies for cancer. This review provides a summary of the essential properties and functional roles of known miRNAs associated with OS in cancers.

scholarly journals Eminence Grise of the Genome: Long Non-Coding Ribonucleic Acids in oral Squamous Cell Carcinomas

2020 ◽  
pp. 35-46
Author(s):  
Dr. Reshma Venugopal ◽  
Dr. Radhika Manoj Bavle ◽  
Dr. Sudhakara Muniswamappa ◽  
Dr. Soumya Makarla
Keyword(s):  
Gene Expression ◽  
Squamous Cell ◽  
Target Gene ◽  
Oral Potentially Malignant Disorders ◽  
Form Complex ◽  
Ribonucleic Acids ◽  
Rna Molecules ◽  
Cellular Processes ◽  
Small Ncrnas ◽  
Potentially Malignant

Non-coding ribonucleic acids (ncRNAs) are a class of RNA molecules that are transcribed but not translated into proteins, but they affect various cellular processes. Around 60% of genes in humans do not code proteins but regulate target gene expression. Presently, a lot of research is carried out on ncRNA involvement in oral squamous cell carcinoma (OSCC) and its precursor lesions termed as oral potentially malignant disorders (OPMDs). They are broadly classified as small ncRNAs (sncRNA) and long ncRNAs (lncRNA). sncRNAs are extensively studied, whereas the divulgence of lncRNAs in OSCCs needs more revelation, hence reviewed in the present article. LncRNAs have a base pair length of more than 200, can form complex structures and influence the gene expression in a multifaceted pattern that attracts interest.

Oxidative Stress and Antioxidants in Neurological Diseases: Is There Still Hope?

2017 ◽  
Vol 18 (6) ◽  
pp. 705-718 ◽  
Author(s):  
Andreia Neves Carvalho ◽  
Omidreza Firuzi ◽  
Maria Joao Gama ◽  
Jack van Horssen ◽  
Luciano Saso
Keyword(s):  
Oxidative Stress ◽  
Neurological Diseases

scholarly journals Targeting Pin1 for Modulation of Cell Motility and Cancer Therapy

Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 359
Author(s):  
Hsiang-Hao Chuang ◽  
Yen-Yi Zhen ◽  
Yu-Chen Tsai ◽  
Cheng-Hao Chuang ◽  
Ming-Shyan Huang ◽  
...  
Keyword(s):  
Cancer Therapy ◽  
Tumor Suppressors ◽  
Protein Conformation ◽  
Genome Stability ◽  
Recent Progress ◽  
Multiple Roles ◽  
Cancer Development ◽  
Cancer Hallmarks ◽  
Underlying Mechanisms ◽  
And Function

Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (Pin1) specifically binds and isomerizes the phosphorylated serine/threonine-proline (pSer/Thr-Pro) motif, which leads to changes in protein conformation and function. Pin1 is widely overexpressed in cancers and plays an important role in tumorigenesis. Mounting evidence has revealed that targeting Pin1 is a potential therapeutic approach for various cancers by inhibiting cell proliferation, reducing metastasis, and maintaining genome stability. In this review, we summarize the underlying mechanisms of Pin1-mediated upregulation of oncogenes and downregulation of tumor suppressors in cancer development. Furthermore, we also discuss the multiple roles of Pin1 in cancer hallmarks and examine Pin1 as a desirable pharmaceutical target for cancer therapy. We also summarize the recent progress of Pin1-targeted small-molecule compounds for anticancer activity.

scholarly journals The biogenesis and biological function of PIWI-interacting RNA in cancer

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Silu Chen ◽  
Shuai Ben ◽  
Junyi Xin ◽  
Shuwei Li ◽  
Rui Zheng ◽  
...  
Keyword(s):  
Cancer Diagnosis ◽  
Precancerous Lesions ◽  
Biological Activities ◽  
Cancer Hallmarks ◽  
Diagnosis And Prognosis ◽  
Small Ncrnas ◽  
Bioinformatics Databases ◽  
Non Coding Rnas ◽  
Underlying Mechanisms ◽  
Proliferative Signaling

AbstractSmall non-coding RNAs (ncRNAs) are vital regulators of biological activities, and aberrant levels of small ncRNAs are commonly found in precancerous lesions and cancer. PIWI-interacting RNAs (piRNAs) are a novel type of small ncRNA initially discovered in germ cells that have a specific length (24–31 nucleotides), bind to PIWI proteins, and show 2′-O-methyl modification at the 3′-end. Numerous studies have revealed that piRNAs can play important roles in tumorigenesis via multiple biological regulatory mechanisms, including silencing transcriptional and posttranscriptional gene processes and accelerating multiprotein interactions. piRNAs are emerging players in the malignant transformation of normal cells and participate in the regulation of cancer hallmarks. Most of the specific cancer hallmarks regulated by piRNAs are involved in sustaining proliferative signaling, resistance to cell death or apoptosis, and activation of invasion and metastasis. Additionally, piRNAs have been used as biomarkers for cancer diagnosis and prognosis and have great potential for clinical utility. However, research on the underlying mechanisms of piRNAs in cancer is limited. Here, we systematically reviewed recent advances in the biogenesis and biological functions of piRNAs and relevant bioinformatics databases with the aim of providing insights into cancer diagnosis and clinical applications. We also focused on some cancer hallmarks rarely reported to be related to piRNAs, which can promote in-depth research of piRNAs in molecular biology and facilitate their clinical translation into cancer treatment.

scholarly journals XBP1-Mediated BiP/GRP78 Upregulation Copes with Oxidative Stress in Mosquito Cells during Dengue 2 Virus Infection

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Tien-Huang Chen ◽  
Yi-Hsuan Chiang ◽  
Jiun-Nan Hou ◽  
Chih-Chieh Cheng ◽  
Eny Sofiyatun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Target Gene ◽  
Cytosolic Calcium ◽  
Cellular Damage ◽  
Factor X ◽  
Stress Indicators ◽  
Mosquito Cells ◽  
Tropical Areas ◽  
Oxidative Stress Indicators ◽  
Denv2 Infection

Dengue viruses (DENVs) cause dengue fever which is an important mosquito-borne disease in tropical areas. Generally, DENV does not cause cellular damage in mosquito cells. However, alterations in cytosolic calcium ions ([Ca2+]cyt) and the mitochondrial membrane potential (MMP), as well as accumulated reactive oxygen species (ROS), including superoxide anions (O2∙-) and hydrogen peroxide (H2O2), can be detected in C6/36 cells with DENV2 infection. Evident upregulation of BiP/GRP78 also appeared at 24 h postinfection in DENV2-infected C6/36 cells. As expression of BiP/GRP78 mRNA was reduced when the transcription factor X-box-binding protein-1 (XBP1) was knocked down in C6/36 cells, it demonstrated that BiP/GRP78 is the target gene regulated by the XBP1 signal pathway. We further demonstrated that the expression and splicing activity of XBP1 were upregulated in parallel with DENV2 infection in C6/36 cells. In C6/36 cells with BiP/GRP78 overexpression, oxidative stress indicators including [Ca2+]cyt, MMP,O2∙-, and H2O2were all pushed back to normal. Taken together, DENV2 activates XBP1 at earlier stage of infection, followed by upregulating BiP/GRP78 in mosquito cells. This regulatory pathway contributes a cascade in relation to oxidative stress alleviation. The finding provides insights into elucidating how mosquitoes can healthily serve as a vector of arboviruses in nature.

393 DECONVOLUTING THE COMPLEXITY OF LONG NON-CODING RNAS AND ESOPHAGEAL CARCINOMA FOR POTENTIAL CLINICAL IMPLICATIONS

2021 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Siyuan Luan ◽  
Yushang Yang ◽  
Shouyue Zhang ◽  
Xiaoxi Zeng ◽  
Xin Xiao ◽  
...  
Keyword(s):  
Esophageal Carcinoma ◽  
Rapid Development ◽  
Direct Interaction ◽  
Clinical Applications ◽  
Regulatory Mechanisms ◽  
Protein Coding ◽  
Functional Roles ◽  
Cancer Hallmarks ◽  
Clinical Scenarios ◽  
Non Coding Rnas

Abstract   Long non-coding RNAs (lncRNAs), a type of transcriptional products with more than 200 nucleotides in length, have been less characterized compared to protein-coding RNAs so far. However, it is increasingly evident that lncRNAs are key players involved in multiple genetic and epigenetic activities during the carcinogenesis of neoplastic diseases. Currently, accumulating data have pointed out the close connection between lncRNAs and esophageal carcinoma (EC), shedding light on further unravelling the complexity of lncRNAs and EC. Methods In this review, we thoroughly collect the evidence regarding original studies on EC-related lncRNAs by searching in MEDLINE/PubMed, Embase and WOS/SCI. We especially focus on summarizing EC-related lncRNAs based upon more updated evidence, and further discuss their different features from various perspectives, including regulatory mechanisms, functional roles in cancer hallmarks, as well as potential diagnostic and therapeutic applications, which would together reveal the complexity of lncRNAs and EC for potential clinical applications. Results We discuss over thirty EC-related lncRNAs in total, most of which function as oncogenes that promote cancer development, while the others function as tumor suppressors. Regulatory mechanisms included sponging miRNAs, direct interaction with proteins, and exosome visicle-based intercellular communication. Based upon these modes of actions, lncRNAs play multiple roles in cancer hallmarks such as uncontrolled cell growth, evasion of programmed cell death, invasion and metastasis. Moreover, lncRNAs packaged in exosomes have unique potency to serve as diagnostic biomarkers; some lncRNAs show great potential to predict patients' chemical resistance and may be crucial targets to improve chemoradiotherapy and targeted therapy. Conclusion Over the past few years, the research of EC-related lncRNAs maintain obviously rapid development, yet further exploration of exact mechanisms and clinical applications that lncRNAs can offer need to be done. Indeed, LncRNAs hold the promise of being applied in multiple clinical scenarios, especially early diagnosis of EC, improvement of sensitivity to chemotherapy/radiotherapy, and development of small-molecule targeted drugs.

Context-specific regulation of lysosomal lipolysis through network-level diverting of transcription factor interactions

2021 ◽  
Vol 118 (41) ◽  
pp. e2104832118
Author(s):  
Vinod K. Mony ◽  
Anna Drangowska-Way ◽  
Reka Albert ◽  
Emma Harrison ◽  
Abbas Ghaddar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Target Gene ◽  
Specific Nature ◽  
C Elegans ◽  
Functional Interactions ◽  
Genetic Epistasis ◽  
Specific Regulation ◽  
Context Specific ◽  
Factor Interactions ◽  
Multicellular Organisms

Plasticity in multicellular organisms involves signaling pathways converting contexts—either natural environmental challenges or laboratory perturbations—into context-specific changes in gene expression. Congruently, the interactions between the signaling molecules and transcription factors (TF) regulating these responses are also context specific. However, when a target gene responds across contexts, the upstream TF identified in one context is often inferred to regulate it across contexts. Reconciling these stable TF–target gene pair inferences with the context-specific nature of homeostatic responses is therefore needed. The induction of the Caenorhabditis elegans genes lipl-3 and lipl-4 is observed in many genetic contexts and is essential to survival during fasting. We find DAF-16/FOXO mediating lipl-4 induction in all contexts tested; hence, lipl-4 regulation seems context independent and compatible with across-context inferences. In contrast, DAF-16–mediated regulation of lipl-3 is context specific. DAF-16 reduces the induction of lipl-3 during fasting, yet it promotes it during oxidative stress. Through discrete dynamic modeling and genetic epistasis, we define that DAF-16 represses HLH-30/TFEB—the main TF activating lipl-3 during fasting. Contrastingly, DAF-16 activates the stress-responsive TF HSF-1 during oxidative stress, which promotes C. elegans survival through induction of lipl-3. Furthermore, the TF MXL-3 contributes to the dominance of HSF-1 at the expense of HLH-30 during oxidative stress but not during fasting. This study shows how context-specific diverting of functional interactions within a molecular network allows cells to specifically respond to a large number of contexts with a limited number of molecular players, a mode of transcriptional regulation we name “contextualized transcription.”

scholarly journals The Role of MicroRNAs in Diabetes-Related Oxidative Stress

2019 ◽  
Vol 20 (21) ◽  
pp. 5423 ◽  
Author(s):  
Mirza Muhammad Fahd Qadir ◽  
Dagmar Klein ◽  
Silvia Álvarez-Cubela ◽  
Juan Domínguez-Bendala ◽  
Ricardo Luis Pastori
Keyword(s):  
Oxidative Stress ◽  
Target Gene ◽  
Cellular Stress ◽  
Cellular Damage ◽  
Oxygen Species ◽  
Non Coding Rnas ◽  
And Oxidative Stress

Cellular stress, combined with dysfunctional, inadequate mitochondrial phosphorylation, produces an excessive amount of reactive oxygen species (ROS) and an increased level of ROS in cells, which leads to oxidation and subsequent cellular damage. Because of its cell damaging action, an association between anomalous ROS production and disease such as Type 1 (T1D) and Type 2 (T2D) diabetes, as well as their complications, has been well established. However, there is a lack of understanding about genome-driven responses to ROS-mediated cellular stress. Over the last decade, multiple studies have suggested a link between oxidative stress and microRNAs (miRNAs). The miRNAs are small non-coding RNAs that mostly suppress expression of the target gene by interaction with its 3’untranslated region (3′UTR). In this paper, we review the recent progress in the field, focusing on the association between miRNAs and oxidative stress during the progression of diabetes.

scholarly journals Protein Carbonylation in Patients with Myelodysplastic Syndrome: An Opportunity for Deferasirox Therapy

Antioxidants ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 508 ◽  
Author(s):  
Alba Rodríguez-García ◽  
María Luz Morales ◽  
Vanesa Garrido-García ◽  
Irene García-Baquero ◽  
Alejandra Leivas ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Target Gene ◽  
Iron Chelator ◽  
Protein Carbonylation ◽  
Fine Tuning ◽  
Self Renewal ◽  
Proliferation And Differentiation ◽  
P53 Target Gene ◽  
And Control

Control of oxidative stress in the bone marrow (BM) is key for maintaining the interplay between self-renewal, proliferation, and differentiation of hematopoietic cells. Breakdown of this regulation can lead to diseases characterized by BM failure such as the myelodysplastic syndromes (MDS). To better understand the role of oxidative stress in MDS development, we compared protein carbonylation as an indicator of oxidative stress in the BM of patients with MDS and control subjects, and also patients with MDS under treatment with the iron chelator deferasirox (DFX). As expected, differences in the pattern of protein carbonylation were observed in BM samples between MDS patients and controls, with an increase in protein carbonylation in the former. Strikingly, patients under DFX treatment had lower levels of protein carbonylation in BM with respect to untreated patients. Proteomic analysis identified four proteins with high carbonylation levels in MDS BM cells. Finally, as oxidative stress-related signaling pathways can modulate the cell cycle through p53, we analyzed the expression of the p53 target gene p21 in BM cells, finding that it was significantly upregulated in patients with MDS and was significantly downregulated after DFX treatment. Overall, our results suggest that the fine-tuning of oxidative stress levels in the BM of patients with MDS might control malignant progression.

scholarly journals Oxidative Stress and the Microbiota-Gut-Brain Axis

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Laura Dumitrescu ◽  
Iulia Popescu-Olaru ◽  
Liviu Cozma ◽  
Delia Tulbă ◽  
Mihail Eugen Hinescu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurological Diseases ◽  
Brain Lesions ◽  
Brain Inflammation ◽  
Oxygen Species ◽  
Mutual Relationship ◽  
Therapeutic Approaches ◽  
Physiological Regulation ◽  
New Therapeutic Approaches ◽  
Important Pathway

The gut-brain axis is increasingly recognized as an important pathway of communication and of physiological regulation, and gut microbiota seems to play a significant role in this mutual relationship. Oxidative stress is one of the most important pathogenic mechanisms for both neurodegenerative diseases, such as Alzheimer’s or Parkinson’s, and acute conditions, such as stroke or traumatic brain injury. A peculiar microbiota type might increase brain inflammation and reactive oxygen species levels and might favor abnormal aggregation of proteins. Reversely, brain lesions of various etiologies result in alteration of gut properties and microbiota. These recent hypotheses could open a door for new therapeutic approaches in various neurological diseases.

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