miRNA as biomarker in lung cancer

Lobera, Esperanza Salcedo; Varela, Macarena Arroyo; Jimenez, Rafael Larrosa; Moreno, Rocio Bautista

doi:10.1007/s11033-023-08695-9

Cited by 8 publications

(2 citation statements)

References 17 publications

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“…Predominantly, miRNAs exhibit imprecise complementarity to target mRNAs, and the degree of complementarity between the miRNA and the mRNA determines the mechanism through which the expression of the target gene is repressed (i.e., mRNA degradation or translation inhibition). Moreover, miRNAs are characterized by their high stability, which supports their use as biomarkers in the realm of clinical diagnostics [40][41][42]. Remarkably, miRNAs are involved in a wide range of biological functions, such as cell differentiation, cell growth, apoptosis, cell proliferation [43,44], tissue regeneration [45], immune responses, inflammation [46], and human reproduction [47,48].…”

Section: Introductionmentioning

confidence: 99%

Exploring the Therapeutic Significance of microRNAs and lncRNAs in Kidney Diseases

Bravo-Vázquez,

Paul,

Colín-Jurado

et al. 2024

Genes

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MicroRNAs (miRNAs) and long non-coding RNAs (lncRNAs) are two crucial classes of transcripts that belong to the major group of non-coding RNAs (ncRNAs). These RNA molecules have significant influence over diverse molecular processes due to their crucial role as regulators of gene expression. However, the dysregulated expression of these ncRNAs constitutes a fundamental factor in the etiology and progression of a wide variety of multifaceted human diseases, including kidney diseases. In this context, over the past years, compelling evidence has shown that miRNAs and lncRNAs could be prospective targets for the development of next-generation drugs against kidney diseases as they participate in a number of disease-associated processes, such as podocyte and nephron death, renal fibrosis, inflammation, transition from acute kidney injury to chronic kidney disease, renal vascular changes, sepsis, pyroptosis, and apoptosis. Hence, in this current review, we critically analyze the recent findings concerning the therapeutic inferences of miRNAs and lncRNAs in the pathophysiological context of kidney diseases. Additionally, with the aim of driving advances in the formulation of ncRNA-based drugs tailored for the management of kidney diseases, we discuss some of the key challenges and future prospects that should be addressed in forthcoming investigations.

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Section: Introductionmentioning

confidence: 99%

Exploring the Therapeutic Significance of microRNAs and lncRNAs in Kidney Diseases

Bravo-Vázquez,

Paul,

Colín-Jurado

et al. 2024

Genes

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show abstract

“…They can regulate the degradation of messenger RNA (mRNA) or suppress the translation through binding to the 3’untranslated region (UTR) of the target mRNA (18). Studies have demonstrated that miRNAs are essential players in a variety of physiological and pathological processes (19–21). Mammalian kidneys can express various miRNAs.…”

Section: Introductionmentioning

confidence: 99%

miR-208a-3p regulated by circUQCRC2 suppresses ischemia/reperfusion-induced acute kidney injury by inhibiting CELF2-mediated tubular epithelial cell apoptosis, inflammation and ferroptosis

Huang,

Meng,

Pang

et al. 2024

Shock

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Background Acute kidney injury (AKI) is a prevalent clinical syndrome with persistent kidney dysfunction. Renal ischemia/reperfusion (I/R) injury is a major cause of AKI. miR-208a-3p overexpression attenuated myocardial I/R injury. This study aims to investigate the role and mechanism of miR-208a-3p in I/R-induced AKI. Methods AKI models were established using hypoxia/reoxygenation (H/R)-exposed tubule epithelial cell HK-2 and I/R-induced mice. The function and mechanism of miR-208a-3p were investigated by gain-or loss-of-function methods using real-time PCR, CCK-8, flow cytometry, ELISA, western blot, hematoxylin-eosin staining, Tunel assay, detection of Fe2+, ROS, BUN and Creatinine, and luciferase reporter assay. Results miR-208a-3p expression was suppressed, while the expression of CELF2 and circular RNA ubiquinol-cytochrome c reductase core protein 2 (circUQCRC2) was increased in both AKI models. miR-208a-3p upregulation or circUQCRC2 silencing increased the viability, decreased the levels of proinflammatory cytokines (TNF-α, IL-1β and IL-6), reduced apoptosis and contents of Fe2+ and ROS, elevated expression of GPX4 and SLC7A11, reduced ACSL4 expression in H/R-stimulated HK-2 cells. Also, miR-208a-3p improved kidney function by alleviating renal injury, apoptosis, inflammation and ferroptosis in AKI mouse model. CELF2 was a target gene of miR-208a-3p which was negatively modulated by circUQCRC2. Overexpression of CELF2 blocked the function of miR-208a-3p upregulation or circUQCRC2 silencing on H/R-treated HK-2 cells. Moreover, the effects of circUQCRC2 downregulation on H/R-injured cells were also reversed by miR-208a-3p inhibitor. Conclusions miR-208a-3p regulated by circUQCRC2 could attenuate I/R-induced AKI by inhibiting CELF2-mediated tubular epithelial cell apoptosis, inflammation and ferroptosis. This study provides potential therapeutic targets for I/R-induced AKI.

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Continuous input DNA Nanomachine to program automated tumor diagnosis and treatment system

Cai,

Wang,

Zhu

et al. 2024

Chemical Engineering Journal

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miRNA as biomarker in lung cancer

Cited by 8 publications

References 17 publications

Exploring the Therapeutic Significance of microRNAs and lncRNAs in Kidney Diseases

Exploring the Therapeutic Significance of microRNAs and lncRNAs in Kidney Diseases

miR-208a-3p regulated by circUQCRC2 suppresses ischemia/reperfusion-induced acute kidney injury by inhibiting CELF2-mediated tubular epithelial cell apoptosis, inflammation and ferroptosis

Continuous input DNA Nanomachine to program automated tumor diagnosis and treatment system

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