scholarly journals Colorectal Adenomas—Genetics and Searching for New Molecular Screening Biomarkers

2020 ◽  
Vol 21 (9) ◽  
pp. 3260 ◽  
Author(s):  
Anna Siskova ◽  
Klara Cervena ◽  
Jan Kral ◽  
Tomas Hucl ◽  
Pavel Vodicka ◽  
...  
Keyword(s):  
Precancerous Lesions ◽  
Colorectal Adenomas ◽  
Inflammatory Factors ◽  
Screening Programs ◽  
Non Invasive ◽  
Asymptomatic Patients ◽  
Non Coding Rna ◽  
Number Of Patients ◽  
Advanced Stages ◽  
Long Non Coding Rna

Colorectal cancer (CRC) is a malignant disease with an incidence of over 1.8 million new cases per year worldwide. CRC outcome is closely related to the respective stage of CRC and is more favorable at less advanced stages. Detection of early colorectal adenomas is the key to survival. In spite of implemented screening programs showing efficiency in the detection of early precancerous lesions and CRC in asymptomatic patients, a significant number of patients are still diagnosed in advanced stages. Research on CRC accomplished during the last decade has improved our understanding of the etiology and development of colorectal adenomas and revealed weaknesses in the general approach to their detection and elimination. Recent studies seek to find a reliable non-invasive biomarker detectable even in the blood. New candidate biomarkers could be selected on the basis of so-called liquid biopsy, such as long non-coding RNA, microRNA, circulating cell-free DNA, circulating tumor cells, and inflammatory factors released from the adenoma into circulation. In this work, we focused on both genetic and epigenetic changes associated with the development of colorectal adenomas into colorectal carcinoma and we also discuss new possible biomarkers that are detectable even in adenomas prior to cancer development.

scholarly journals Long Non-Coding RNA in Vascular Disease and Aging

2019 ◽  
Vol 5 (1) ◽  
pp. 26 ◽  
Author(s):  
Diewertje Bink ◽  
Noelia Lozano-Vidal ◽  
Reinier Boon
Keyword(s):  
Cardiovascular Diseases ◽  
Vascular Disease ◽  
Vascular Diseases ◽  
The Elderly ◽  
Western Society ◽  
Non Coding Rna ◽  
Number Of Patients ◽  
Non Coding Rnas ◽  
Near Future ◽  
Long Non Coding Rna

Cardiovascular diseases are the most prominent cause of death in Western society, especially in the elderly. With the increasing life expectancy, the number of patients with cardiovascular diseases will rise in the near future, leading to an increased healthcare burden. There is a need for new therapies to treat this growing number of patients. The discovery of long non-coding RNAs has led to a novel group of molecules that could be considered for their potential as therapeutic targets. This review presents an overview of long non-coding RNAs that are regulated in vascular disease and aging and which might therefore give insight into new pathways that could be targeted to diagnose, prevent, and/or treat vascular diseases.

scholarly journals Long non-coding RNA NEAT1 aggravates epilepsy and seizure-induced neuronal damage by regulating microRNA-139/ROCK1 axis

2020 ◽  
Author(s):  
Xiaowan Li ◽  
Fang Hao ◽  
Shuxin Tao ◽  
Weihua Wang ◽  
Xinxing Xiao ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Hippocampal Neurons ◽  
Neuronal Damage ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Endogenous Expression ◽  
Non Coding Rna ◽  
Gene Assay ◽  
Lncrna Neat1 ◽  
Long Non Coding Rna

Abstract Background Both long non-coding RNA (lncRNA) NEAT1 and microRNA (miR)-139 are crucial gene regulators in various disorders. This study aims to investigate their role in epilepsy and seizure-induced neuronal damage. Methods In this research, rat model of epilepsy was established by pilocarpine induction. The RNA and protein expression in hippocampal tissues and neurons were determined by RT-qPCR and Western blot analysis, respectively. Microarray analysis was used to predict the relationship between NEAT1 and miR-139 or between miR-139 and ROCK1, and dual luciferase reporter gene assay was performed to verify the interaction. The endogenous expression of related genes was modulated by recombinant plasmids and cell transfection. The cell apoptosis, levels of inflammatory factors and cell proliferation were detected by flow cytometry, ELISA and EdU assay. Results LncRNA NEAT1 and ROCK1 was upregulated, while the miR-139 was downregulated in hippocampal tissues and neurons of epileptic rats. Overexpression of NEAT1 decreased the activity of neurons, increased cell apoptosis, and increased the level of inflammatory factors. NEAT1 negatively targeted miR-139 to upregulate ROCK1. The RhoA/ROCK1 signaling pathway was activated by NEAT1 overexpression and miR-139 downregulation. Conclusion LncRNA NEAT1 suppressed pilocarpine-induced epilepsy by inhibiting apoptosis of hippocampal neurons through miR-139/RhoA/ROCK1 axis, and thereby inhibiting neuronal injury induced by seizure.

scholarly journals CANCER AND COVID-19. A COMBAT STRATEGY

2021 ◽  
Vol 65 (2) ◽  
Author(s):  
Nazar Lukavetskyy ◽  
◽  
Nataliya Volod'ko ◽  
Keyword(s):  
Public Health ◽  
Cancer Patients ◽  
European Society ◽  
Medical Oncology ◽  
Health Problems ◽  
Medical Industry ◽  
Negative Effects ◽  
Screening Programs ◽  
Number Of Patients ◽  
Advanced Stages

Strict quarantine measures and the unpreparedness of the medical industry have exacerbated public health problems on all continents. The number of patients with advanced stages of cancer has increased at the end of the year. Several approaches could mitigate the negative effects of Covid-19 on screening programs. International oncology organization «European Society of Medical Oncology» (ESMO) has launched a section COVID 19 on its website. We believe that some aspects of the ESMO recommendations should be widely presented. The feasibility of vaccinating cancer patients against COVID-19 is undeniable

scholarly journals Targeting MALAT1 and miRNA-181a-5p for the intervention of acute lung injury/acute respiratory distress syndrome

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Yaling Liu ◽  
Xiaodong Wang ◽  
Peiying Li ◽  
Yanhua Zhao ◽  
Liqun Yang ◽  
...  
Keyword(s):  
Lung Injury ◽  
Vascular Inflammation ◽  
Inflammatory Factors ◽  
Microvascular Endothelial Cell ◽  
High Morbidity ◽  
Therapeutic Effects ◽  
Non Coding Rna ◽  
Pulmonary Microvascular Endothelial Cell ◽  
Long Non Coding Rna

Abstract Background ALI/ARDS is a severe lung injury leading to refractory respiratory failure, accounting for high morbidity and mortality. However, therapeutic approaches are rather limited. Targeting long non-coding RNA MALAT1 and microRNA miR-181a-5p might be potential option for ALI/ARDS intervention. Objective We aimed to investigate the role of MALAT and miR-181a-5p in the pathogenesis of ALI/ARDS, and test the therapeutic effects of targeting MALAT and miR-181a-5p for ALI/ARDS intervention in vitro. Methods MALAT1 and miR-181a-5p levels were measured in plasma from ALI/ARDS patients. In vitro human pulmonary microvascular endothelial cell (HPMEC) injury was induced by LPS treatment, and molecular targets of MALAT1 and miR-181a-5p were explored by molecular biology approaches, mainly focusing on cell apoptosis and vascular inflammation. Interaction between MALAT1 and miR-181a-5p was also detected. Finally, the effects of targeting MALAT1 and miR-181a-5p for ALI/ARDS intervention were validated in a rat ALI/ARDS model. Results MALAT1 upregulation and miR-181a-5p downregulation were observed in ALI/ARDS patients. Transfection of mimic miR-181a-5p into HPMECs revealed decreased Fas and apoptosis, along with reduced inflammatory factors. Fas was proved to be a direct target of miR-181a-5p. Similar effects were also present upon MALAT1 knockdown. As for the interaction between MALAT1 and miR-181a-5p, MALAT1 knockdown increased miR-181a-5p expression. Knocking down of MALAT1 and miR-181a-5p could both improve the outcome in ALI/ARDS rats. Conclusion MALAT1 antagonism or miR-181a-5p could both be potential therapeutic strategies for ALI/ARDS. Mechanistically, miR-181a-5p directly inhibits Fas and apoptosis, along with reduced inflammation. MALAT1 negatively regulates miR-181a-5p.

scholarly journals LINC01534 promotes the aberrant metabolic dysfunction and inflammation in IL-1β-simulated osteoarthritic chondrocytes by targeting miR-140-5p

2019 ◽  
Author(s):  
Wei Wei ◽  
Shaoxuan He ◽  
Zhihua Wang ◽  
Junjie Dong ◽  
Dong Xiang ◽  
...  
Keyword(s):  
Inhibitory Effect ◽  
Cartilage Tissue ◽  
Inflammatory Factors ◽  
Metabolic Dysfunction ◽  
Matrix Degradation ◽  
Non Coding Rna ◽  
Osteoarthritic Chondrocytes ◽  
Tnf Α ◽  
Collagen Ii ◽  
Long Non Coding Rna

Abstract Backgrounds: Long non-coding RNA 01534 (LINC01534) is highly expressed in the tissues of patients with osteoarthritis (OA). This study investigated the mechanism of LINC01534 on abnormal metabolic dysfunction and inflammation in OA chondro-cytes induced by IL-1β. Methods: The quantitative Real-Time PCR (qRT-PCR) was used to determine the expressions of LINC01534, aggrecan, collagen II and matrix metalloproteinase (MMPs) in OA cartilage tissue or OA chondrocyte model induced by IL-1β. The ex-pressions of aggrecan and collagen II in the chondrocyte were detected by Western Blot. The levels of TNF-α, IL-8, IL-6, MMP-13, MMP-9, MMP-3 and prostaglandin E2 (PGE2) in chondrocyte were determined by ELISA. Bioinformatics, dual luciferin gene reporting, RNA pulldown and Northern Blot were used to determine the interac-tion between LINC01534 and miR-140-5p. Results: The results showed that LINC01534 was up-regulated in both OA cartilage tissue and OA chondrocyte model. In addition, silencing LINC01534 significantly alleviated the inhibitory effect of IL-1β on expressions of aggrecan and collagen II in chondrocytes, and significantly down-regulated the expression of matrix metallopro-teinases in IL-1β-induced chondrocytes. Meanwhile, silencing LINC01534 also sig-nificantly inhibited the productions of pro-inflammatory factors NO, PGE2, TNF-α, IL-6 and IL-8 in the IL-1β-induced chondrocytes. Furthermore, miR-140-5p was con-firmed to be a direct target of LINC01534. More importantly, inhibition of miR-140-5p significantly reversed the inhibitory effect of silencing LINC01534 on inflammation and abnormal matrix degradation in the IL-1β-induced chondrocyte model of OA. Conclusion: Therefor, LINC01534 could promote the abnormal matrix degradation and inflammatory response of OA chondrocytes through the targeted binding of miR-140-5p.

scholarly journals Definition and review on a category of long non-coding RNA: Atherosclerosis-associated circulating lncRNA (ASCLncRNA)

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e10001
Author(s):  
Shanshan Lu ◽  
Qin Liang ◽  
Yanqing Huang ◽  
Fanming Meng ◽  
Junwen Liu
Keyword(s):  
Noncoding Rnas ◽  
Circulatory System ◽  
Modern Society ◽  
Apoptotic Bodies ◽  
Non Invasive ◽  
Physiological Processes ◽  
Non Coding Rna ◽  
Definition Of ◽  
Long Non Coding Rna ◽  
Potential Biomarkers

Atherosclerosis (AS) is one of the most common cardiovascular system diseases which seriously affects public health in modern society. Finding potential biomarkers in the complicated pathological progression of AS is of great significance for the prevention and treatment of AS. Studies have shown that long noncoding RNAs (lncRNAs) can be widely involved in the regulation of many physiological processes, and have important roles in different stages of AS formation. LncRNAs can be secreted into the circulatory system through exosomes, microvesicles, and apoptotic bodies. Recently, increasing studies have been focused on the relationships between circulating lncRNAs and AS development. The lncRNAs in circulating blood are expected to be new non-invasive diagnostic markers for monitoring the progression of AS. We briefly reviewed the previously reported lncRNA transcripts which related to AS development and detectable in circulating blood, including ANRIL, SENCR, CoroMarker, LIPCAR, HIF1α-AS1, LncRNA H19, APPAT, KCNQ1OT1, LncPPARδ, LincRNA-p21, MALAT1, MIAT, and UCA1. Further researches and a definition of atherosclerosis-associated circulating lncRNA (ASCLncRNA) were also discussed.

scholarly journals Telomeric repeat-containing ribonucleic acid (TERRA) expression in patients with idiopathic pulmonary fibrosis

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Manal M. El-Desoky ◽  
Asem A. Hewidy ◽  
Ahmed M. Fouda ◽  
Fatma Azzahraa Hisham
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Telomeric Repeat ◽  
Expression Level ◽  
Strongly Correlated ◽  
High Resolution Computed Tomography ◽  
Non Invasive ◽  
Non Coding Rna ◽  
Extent Score ◽  
Long Non Coding Rna

Abstract Background Idiopathic pulmonary fibrosis (IPF) represents a chronic disease with a progressive course. It is characterized by excessive lung scarring that ultimately contributes to irreversible lung function reduction. Interestingly, a type of long non-coding RNA termed as telomeric repeat-containing RNA (TERRA) is linked to fibrosis pathophysiology, including IPF. In this study, the expression profile of TERRA was investigated in IPF patients on radiological diagnosis [unusual interstitial pattern (UIP) in high-resolution computed tomography (HRCT)] to evaluate whether it could be employed as a reliable diagnostic biomarker. Results TERRA expression level was significantly higher in IPF patients over healthy controls. The expression level was significantly inversely correlated with the percentage of forced vital capacity predicted (FVC% predicted). By contrast, it was significantly directly correlated with HRCT reticular extent score. Conclusion TERRA expression is an essential biomarker in peripheral blood of IPF patients, providing a valuable non-invasive tool for IPF diagnosis. Moreover, TERRA expression is strongly correlated with UIP in HRCT reticular extent score.

scholarly journals Long Non-Coding RNA DANCR Participates in the Regulation of Dexamethasone and Inflammation Factors on hASC Proliferation and Migration

2021 ◽  
Author(s):  
Ran Yan ◽  
Ping Dong ◽  
Zhigang Yang ◽  
Rui Cao ◽  
Xia Liu ◽  
...  
Keyword(s):  
Cell Counting ◽  
Inflammatory Factors ◽  
Dependent Manner ◽  
Migration Ability ◽  
Non Coding Rna ◽  
Tnf Α ◽  
The Mean ◽  
And Migration ◽  
Long Non Coding Rna ◽  
Proliferation And Migration

Abstract BackgroundBoth MSC and Dexamethasone are effective methods to treat inflammatory diseases, and they are likely to be used in combination. The proliferation and migration ability is one of the main biological characteristics of MSC for repairing. However, the effect of inflammatory factors and Dex on these characteristics of MSC has not been fully understood. Therefore, this study aimed to determine the role of lncRNA DANCR in hASC proliferation and migration regulation induced by Dex and inflammatory factors, to clarify the effect and mechanism of glucocorticoids on MSC's characteristics to participate in tissue repair in an inflammatory environment. MethodshASCs were cultured and treated with dexamethasone and inflammation factors, and cell proliferation, migration abilities, and lncRNA DANCR mRNA expression were detected. Additionally, to determine the roles and mechanisms, lncRNA DANCR was knockdown or overexpressed before Dex or TNF-α treatments. MSC proliferation was tested by cell counting kit-8 and cell cycle assay. MSC migration ability was analyzed by a scratching test. Moreover, proliferation and migration-related genes were measured by a reverse transcription-polymerase chain reaction. Nuclear factor-kB (NF-κB) and PI3K-AKT-mTOR pathway proteins were investigated by western blot analysis. All values are expressed as the mean ± standard error of the mean. The differences between the groups were assessed using a two-tailed Student’s t-test. ResultsDex decreased the proliferation and migration of hASC in a dose-dependent manner. Dex could upregulate the expression of lncRNA DANCR that inhibited hASC proliferation and migration. Knockdown of DANCR reversed the inhibition of hASC proliferation and migration induced by Dex. Moreover, DANCR was decreased by inflammatory cytokines, and overexpression of DANCR alleviated the promotion of hASC proliferation and migration induced by TNF-α. Furthermore, mechanistic investigation validated that DANCR was involved in the NF-κB signaling pathway. ConclusionsWe identified a lncRNA, DANCR, involved in Dex and inflammation-affected hASC proliferation and migration, thus suggesting that concurrent application of hASCs with steroids should be avoided in clinical settings. DANCR may serve as a promising approach to regulate stem cell characteristics under an inflamed microenvironment. These findings further enrich our understanding of the functional versatility of lncRNAs in the crosstalk of inflammation conditions and stem cells. Keywords： DANCR; long non-coding RNA; Dexamethasone; TNF-α; hASC; proliferation; migration

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