miRNA dysregulation is an emerging modulator of genomic instability

Cardoso, Ana Paula Ferragut; Banerjee, Minakshi; Nail, Alexandra N.; Lykoudi, Angeliki; States, J. Christopher

doi:10.1016/j.semcancer.2021.05.004

Cited by 64 publications

(45 citation statements)

References 170 publications

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“…Recent studies have reported that miR-21-3p overexpression can induce microsatellite instability by targeting MSH2 , a key mismatch repair gene. [ 74 ]…”

Section: Discussionmentioning

confidence: 99%

MiRNA expression profiling in adenocarcinoma and squamous cell lung carcinoma reveals both common and specific deregulated microRNAs

et al. 2022

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The current study investigated the expression signatures of miRNAs in lung adenocarcinoma (LUAD) and squamous cell lung carcinoma (LUSC). miRNA profiling was performed using microarray in 12 LUAD and 12 LUSC samples and adjacent normal tissues. In LUAD, 107 miRNAs were significantly deregulated, whereas 235 miRNAs were deregulated in LUSC. Twenty-six miRNAs were common between the 2 cancer subtypes and 8 were prioritized for validation, in addition to 6 subtype-specific miRNAs. The RT-qPCR validation samples included 50 LUAD, 50 LUSC, and adjacent normal tissues. Eight miRNAs were validated in LUAD: 3 upregulated -miR-7-5p, miR- 375-5p, miR-6785-3p, and 5 downregulated -miR-101-3p, miR-139-5p, miR-140-3p, miR-144-3p, miR-195-5p. Ten miRNAs were validated in the LUSC group: 3 upregulated -miR-7-5p, miR-21-3p, miR-650, and 7 downregulated -miR- 95-5p, miR-140-3p, miR-144-3p, miR-195-5p, miR-375, miR-744-3p, and miR-4689-3p. Reactome pathway analysis revealed that the target genes of the deregulated miRNAs in LUAD were significantly enriched in cell cycle, membrane trafficking, gene expression processes, and EGFR signaling, while in LUSC, they were enriched in the immune system, transcriptional regulation by TP53, and FGFR signaling. This study identified distinct miRNA profiles in LUSC and LUAD, which are common and specific miRNAs that could be further investigated as biomarkers for diagnosis and prognosis.

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“…Recent studies have reported that miR-21-3p overexpression can induce microsatellite instability by targeting MSH2 , a key mismatch repair gene. [ 74 ]…”

Section: Discussionmentioning

confidence: 99%

MiRNA expression profiling in adenocarcinoma and squamous cell lung carcinoma reveals both common and specific deregulated microRNAs

et al. 2022

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“…These reverse-spliced molecules are divided into exon, intron, and exon–intron circRNAs [ 12 , 15 ]. MiRNAs, ranging from 21 to 24 nucleotides in length, are a class of conserved non-coding RNA molecules [ 16 ]. The first miRNA was discovered in 1993 which was 13 years after the discovery of circRNA [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

A novel circRNA, hsa_circ_0069382, regulates gastric cancer progression

et al. 2023

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Aberrant expression of circRNAs is closely associated with the progression of gastric cancer; however, the specific mechanisms involved remain unclear. Our aim was to identify new gastric cancer biomarkers and explore the molecular mechanisms of gastric cancer progression. Therefore, we analyzed miRNA and circRNA microarrays of paired early-stage gastric cancer samples. Our study identified a new circRNA called hsa_circ_0069382, that had not been reported before and was expressed at low levels in gastric cancer tissues. Our study also included bioinformatics analyses which determined that the high expression of hsa_circ_0069382 regulated the BTG anti-proliferation factor 2 (BTG2)/ focal adhesion kinase (FAK) axis in gastric cancer lines by sponging for miR-15a-5p. Therefore, proliferation, invasion, and migration of gastric cancer is impacted. miR-15a-5p overexpression partially restored the effects of hsa_circ_0069382. This study provides potential new therapeutic options and a future direction to explore for gastric cancer treatment, and biomarkers. Graphical Abstract

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“…Evidence suggests that MVs can ameliorate renal injury by delivering miRNAs [ 13 , 14 ]. It is well known that dysregulated miRNAs can affect the occurrence and development of various diseases [ 15 , 16 ], including HN [ 17 ]. miRNAs affect renal function by binding to the 3′-UTR of downstream mRNAs and regulating mRNA transcription and translation [ 18 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

Endothelial Progenitor Cells Affect the Growth and Apoptosis of Renal Cells by Secreting Microvesicles Carrying Dysregulated miR-205 and miR-206

et al. 2023

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Background. This study investigated the mechanism of microRNA (miRNA, miR) in microvesicles (MVs) secreted by endothelial progenitor cells (EPCs) involved in renal function in vivo and in vitro injury repair of rat primary kidney cells (PRKs). Methods. Gene Expression Omnibus analysis of potential target miRNAs in nephrotic rats. Real-time quantitative polymerase chain reaction verified the correlation of these miRNAs and screened the effective target miRNAs and their downstream putative target mRNAs. Western blot analyzes the protein levels of DEAD-box helicase 5 (DDX5) and the activation of the proapoptotic factor caspase-3/9 (cleaved). Dil-Ac-LDL staining, immunofluorescence, and a transmission electron microscope (TEM) were used to identify the successful isolation of EPCs and PRKs and the morphology of MVs. Cell Counting Kit-8 was used to detect the effect of miRNA-mRNA on the proliferation of PRKs. Standard biochemical kits were used to detect biochemical indicators in rat blood and urine. Dual-luciferase analysis of miRNA binding to mRNA was conducted. The effect of miRNA-mRNA interaction on the apoptosis level of PRKs was analyzed by flow cytometry. Results. A total of 13 rat-derived miRNAs were potential therapeutic targets, and miR-205 and miR-206 were screened as the targets of this study. We found that the EPC-MVs alleviated the increase of blood urea nitrogen and urinary albumin excretion and the decrease in creatinine clearance caused by hypertensive nephropathy in vivo. The effect of MVs in improving renal function indicators was promoted by miR-205 and miR-206 and inhibited by knockdown of expressed miR-205 and miR-206. In vitro, angiotensin II (Ang II) promoted growth inhibition and apoptosis of PRKs, and similarly, dysregulated miR-205 and miR-206 affected the induction of Ang II. We then observed that miR-205 and miR-206 cotargeted the downstream target DDX5 and regulated its transcriptional activity and translational levels, while also reducing the activation of proapoptotic factors caspase-3/9. Overexpressed DDX5 reversed the effects of miR-205 and miR-206. Conclusion. By upregulating the expression of miR-205 and miR-206 in MVs secreted by EPC, the transcriptional activity of DDX5 and the activation of caspase-3/9 can be inhibited, thereby promoting the growth of PRKs and protecting the injury caused by hypertensive nephropathy.

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miRNA dysregulation is an emerging modulator of genomic instability

Cited by 64 publications

References 170 publications

MiRNA expression profiling in adenocarcinoma and squamous cell lung carcinoma reveals both common and specific deregulated microRNAs

MiRNA expression profiling in adenocarcinoma and squamous cell lung carcinoma reveals both common and specific deregulated microRNAs

A novel circRNA, hsa_circ_0069382, regulates gastric cancer progression

Endothelial Progenitor Cells Affect the Growth and Apoptosis of Renal Cells by Secreting Microvesicles Carrying Dysregulated miR-205 and miR-206

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