Potential functions of hsa-miR-155-5p and core genes in chronic myeloid leukemia and emerging role in human cancer: A joint bioinformatics analysis

Soltani, Ismael; Bahia, Wael; Farrah, Ahlem; Mahdhi, Abdelkarim; Ferchichi, Salima; Almawi, Wassim Y.

doi:10.1016/j.ygeno.2021.04.014

Cited by 8 publications

(4 citation statements)

References 80 publications

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“…Hsa-mir-21-5p is a carcinogenic miRNA and overexpressed in many human malignancies such as acute myeloid leukemia (AML), lung, brain and breast cancer (Si et al, 2007;Bourguignon et al, 2009;Liu et al, 2021). Similarly, many studies reported overexpression of hsa-mir-155-5p in most solid and hematological malignancies (Liu et al, 2014;Robertson et al, 2014;Baba et al, 2016;Zeng et al, 2016;Pagotto et al, 2018Pagotto et al, , 2019Soltani et al, 2021), B-cell chronic lymphocytic leukemia (Cui et al, 2013;Ferrajoli et al, 2014;Due et al, 2016;Pagotto et al, 2019), and CLL Ferrajoli et al (2014). The upregulation of hsa-mir-155-5p was associated with subsequent risk of CLL (Balatti et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

Identification of microRNA editing sites in three subtypes of leukemia

Xie

Yang²,

Zhou

et al. 2022

Front. Mol. Biosci.

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Leukemia is an aberrant hyper-proliferation of immature blood cells that do not form solid tumors. The transcriptomes of microRNAs (miRNAs) of leukemia have been intensively explored. However, miRNA editing of leukemia has not been extensively studied. To identify miRNA editing patterns and explore their functional relevance in leukemia, we analyzed 200 small RNA sequencing profiles of three subtypes of leukemia and identified hundreds of miRNA editing sites in three subtypes of leukemia. Then, we compared the editing levels of identified miRNA editing sites in leukemia and normal controls. Many miRNAs were differential edited in different subtypes of leukemia. We also found the editing levels of 3′-A editing sites of hsa-mir-21-5p and hsa-mir-155-5p decreased in chronic lymphocytic leukemia patients with radiation treatments. By integrating PAR-CLIP sequencing profiles, we predicted the targets of original and edited miRNAs. One of the edited miRNA, hsa-let-7b_5c, with an additional cytosine at 5′ end of hsa-let-7b-5p, potentially targeted VBP1 and CTDSP1. CTDSP1 was significantly downregulated in T-ALL compared to normal controls, which might be originated from the hyperediting of hsa-let-7b-5p in T-ALL. Our study provides a comprehensive view of miRNA editing in three different subtypes of leukemia.

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Section: Discussionmentioning

confidence: 99%

Identification of microRNA editing sites in three subtypes of leukemia

Xie

Yang²,

Zhou

et al. 2022

Front. Mol. Biosci.

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“…Cancer is driven by the hyperactivity of cancer-promoting oncogenes and/or the inactivation of tumor suppressor genes [38]. While clinicopathological and clinical variables are helpful in predicting cancer outcomes, the characterization of solid cancers relies on invasive biopsies and/or open surgical sampling.…”

Section: Discussionmentioning

confidence: 99%

Utility of Circulating Cell-Free DNA in Assessing Microsatellite Instability and Loss of Heterozygosity in Breast Cancer Using Human Identification Approach

Sharhan

Messaoudi

Babu

et al. 2022

Genes

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The diagnostic and prognostic utility of circulating cell-free DNA (cfDNA) in breast cancer (BC) patients was recently reported. Here, we investigated the use of cfDNA to examine microsatellite instability (MSI) and loss of heterozygosity (LOH) for early BC diagnosis. cfDNA and genomic DNA from 41 female BC patients and 40 healthy controls were quantified using NanoDrop spectrophotometry and real-time PCR. The stability of genomic and cfDNA was assessed using a high-resolution AmpFlSTR MiniFiler human identification kit. Significant increases in cfDNA plasma concentrations were observed in BC patients compared to controls. The genotype distribution of the eight autosomal short tandem repeat (STR) loci D7S820, D13S317, D21S11, D2S1338, D18S51, D16S539, FGA, and CSF1PO were in Hardy–Weinberg equilibrium. Significant differences in the allele frequencies of D7S820 allele-8, D21S11 allele-29, allele-30.2, allele-32.2, and CSF1PO allele-11 were seen between BC patients and controls. LOH and MSI were detected in 36.6% of the cfDNA of patients compared to genomic DNA. This study highlights the utility of plasma-derived cfDNA for earlier, less invasive, and cost-effective cancer diagnosis and molecular stratification. It also highlights the potential value of cfDNA in molecular profiling and biomarkers discovery in precision and forensic medicine.

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“…Further, we analyzed the TF-miRNA coregulatory network of the 20 hub genes, and we found that miR-155-5p with the highest network betweenness could regulate the expression of FLT1, CXCL8, JUN, THBS1, ICAM1, CD34, and FGF13. It has been reported that miR-155-5p is a key oncogenic microRNA that maintains immune homeostasis and mediates cross-talk between in ammation and tumorigenesis [42]. Previous studies have indicated that miR-155-5p is highly expressed in many cancers, such as lung cancer, breast cancer, colon cancer, lymphoma, and other tumors [43,44].…”

Section: Discussionmentioning

confidence: 99%

Identification of key genes of anti-programmed death ligand 1 for meningioma immunotherapy by bioinformatic analysis

Zhang

Wang

Tan

et al. 2022

Preprint

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Meningioma is one of the most common primary tumors in the central nervous system (CNS). A deeper understanding of its molecular characterization could provide potential therapeutic targets to reduce recurrence. In this study, we attempted to identify specific gene mutations in meningioma for immunotherapy. One GSE43290 dataset was obtained from the Gene Expression Omnibus (GEO) database to find differentially expressed genes (DEGs) between meningioma tissues and normal meninges. In total, 420 DEGs were identified, including 15 up-regulated and 405 down-regulated genes. Functional enrichment analysis showed that these DEGs were mainly enriched in PI3K-Akt signaling pathway, Focal adhesion, and MAPK signaling pathway. We identified 20 hub genes by protein-protein interaction (PPI) analysis. Among the hub genes, the expression of FLT1, CXCL8, JUN, THBS1, FECAM1, CD34, and FGF13 were negatively correlated with Programmed Death Ligand-1 (PD-L1). Additionally, the expression of those genes was co-regulated by miR-155‐5p. The findings suggest that miR-155-5p play an important role in the pathogenesis of meningioma and may represent potential therapeutic targets for its anti-PD-L1 immunotherapy.

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Potential functions of hsa-miR-155-5p and core genes in chronic myeloid leukemia and emerging role in human cancer: A joint bioinformatics analysis

Cited by 8 publications

References 80 publications

Identification of microRNA editing sites in three subtypes of leukemia

Identification of microRNA editing sites in three subtypes of leukemia

Utility of Circulating Cell-Free DNA in Assessing Microsatellite Instability and Loss of Heterozygosity in Breast Cancer Using Human Identification Approach

Identification of key genes of anti-programmed death ligand 1 for meningioma immunotherapy by bioinformatic analysis

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