Abnormal microRNA expression in the course of hematological malignancies

Szymczyk, Agnieszka; Macheta, Arkadiusz; Podhorecka, Monika

doi:10.2147/cmar.s174476

Cited by 35 publications

(26 citation statements)

References 111 publications

(140 reference statements)

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“…miRNAs are capable of regulating gene expression at the transcriptional or post-transcriptional level by partially base pairing with the 3′-untranslated regions (3′-UTRs) of their target genes, triggering mRNA degradation, and/or transcriptional silencing 11. Aberrations in miRNA expression have been reported in nearly all types of human cancer, suggesting that miRNAs participate in carcinogenesis and cancer progression 12–14. Promising studies have discovered that various miRNAs are dysregulated in PTC and exert tumor-suppressive or oncogenic roles 15–17.…”

Section: Introductionmentioning

confidence: 99%

microRNA-564 inhibits the aggressive phenotypes of papillary thyroid cancer by directly targeting astrocyte-elevated gene-1

Song

Yang

et al. 2019

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Background: Accumulating evidence has revealed that an increasing number of microRNAs (miRNAs) are dysregulated in papillary thyroid cancer (PTC) and that their dysregulation plays an important role in PTC onset and progression. Reportedly, miRNA-564 (miR-564) is downregulated in several types of human cancer. However, its expression profile and specific functions in PTC remain unclear to date. Methods: In this study, we used reverse transcription-quantitative polymerase chain reaction to detect miR-564 expression in PTC tissues and cell lines. Further, the regulatory roles of miR-564 in the malignant development of PTC in vitro and in vivo were examined using a series of functional experiments. In addition, the possible underlying mechanisms and signaling pathways involved were investigated. Results: We demonstrated that miR-564 expression markedly decreased in PTC tissues and cell lines, and this decrease correlated with the lymph node metastasis and tumor–node–metastasis stage. miR-564 upregulation significantly inhibited cell proliferation, migration, and invasion and induced cell apoptosis in vitro as well as hindered tumor growth in vivo. Furthermore, astrocyte-elevated gene-1 (AEG-1) was identified as a direct target gene of miR-564 in PTC cells. Its expression was upregulated and inversely correlated with miR-564 expression in clinically PTC tissues. Additionally, the silencing of AEG-1 expression could imitate the action of miR-564 overexpression in PTC cells. Remarkably, the restoration of AEG-1 expression partially abolished the tumor-suppressing effects induced by a miR-564 upregulation in PTC cells. Ectopic miR-564 expression deactivated the PTEN/Akt pathway in PTC cells in vitro and in vivo. Conclusion: Overall, the findings of the current study suggest that miR-564 is a tumor-suppressive miRNA that exerts crucial roles in the development and progression of PTC. Therefore, this miRNA might be a promising candidate target in the anticancer treatment of patients with PTC.

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Section: Introductionmentioning

confidence: 99%

microRNA-564 inhibits the aggressive phenotypes of papillary thyroid cancer by directly targeting astrocyte-elevated gene-1

Song

Yang

et al. 2019

OTT

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“…Micro RNA (miRNA) is an endogenous small non-coding RNA, which inhibits the expression of target genes by inhibiting the translation or increasing the degradation of mRNA, and plays a wide range of biological functions in cell proliferation, apoptosis, invasion, differentiation, and other important cellular processes 19. More than 30% of human genes can be regulated by various miRNAs, and it has been confirmed that abnormal miRNA expression is involved in the tumorigenesis and development of numerous malignancies 20,21…”

Section: Introductionmentioning

confidence: 99%

Downregulation of microRNA-4324 promotes the EMT of esophageal squamous-cell carcinoma cells via upregulating FAK

Zhou¹,

Zhu²,

Jiang³

et al. 2019

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Background: Esophageal squamous-cell carcinoma (ESCC) metastasis is the major cause of death of this severe and common malignancy. Focal adhesion kinase (FAK) is one of the key components of the focal adhesion complex, which is a multi-protein structure that controls cell adhesion, migration and invasion and regulates tumor metastasis. Purpose: To identify the roles and mechanisms of FAK in the regulation of Epithelial-to-mesenchymal transition (EMT) of ESCC cells. Methods: The expression of FAK and miR-4324 in both ESCC tissues and cells were evaluated by qRT-PCR and Immunohistochemistry analysis. Dual luciferase assays were performed for the confirmation of miR-4324’s specific binding to 3’UTR of FAK mRNA. Besides, the trans-well assays and wound healing assays were employed to evaluate the effects of FAK /miR-4324 axis on the EMT regulation of ESCC cells. Furthermore, the relationship between miR-4374/FAK expression and clinical pathologic parameters & patient survival were also statistically analyzed. Results: In this study, we identified the upregulation of FAK and downregulation of miR-4324 in both ESCC cells and tissues. Overexpression of miR-4324 mimic, which significantly decreased cellular FAK levels, can impair the invasion potential and migration ability of ESCC cells. Besides, co-transfection of FAK can attenuate the function of miR-4324 mimic. Further experimental results demonstrated that miR-4324 mimic remarkably downregulated epithelial-to-mesenchymal transition (EMT) phenotype, which can also be effectively prevented by overexpressing FAK in ESCC cells. What’s more, low miR-4324 and high FAK tissue levels have significant association with poor cell differentiation, tumor size and invasion depth as well as overall number of metastatic lymph nodes. Patients with high miR-4324 and low FAK levels in tumoral tissues lived longer than their counterparts, respectively. Conclusions: In conclusion, miR-4324/FAK axis could be a promising therapeutic target and potential prognostic biomarker for ESCC, which deserves further investigation in the clinic.

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“…Inhibiranjem određenih miRNK može doći do redukcije tumorske proliferacije. [48][49][50][51][52][53] Prvi mikroRNK biofarmaceutik jest MRX34, trenutačno jedini čija se djelotvornost ispituje u onkološkim kliničkim istraživanjima (faza 1). 54 Područje istraživanja ovih malenih, nekodirajućih miRNK golemo je i raste iz dana u dan donoseći nam nove spoznaje o njihovoj važnosti u patogenezi različitih tumora.…”

Section: Izražaj Mirnk U Mds-uunclassified

CIRCULATING microRNA EXPRESSION IN MYELODYSPLASTIC SYNDROME

2019

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Myelodysplastic syndrome (MDS) is a clonal hematopoietic stem cell disorder characterized by ineffective hematopoiesis and cytopenia in peripheral blood, where about a third of patients may develop acute myeloid leukemia (AML). The diagnosis of MDS requires the analysis of peripheral blood and bone marrow. Depending on the percentage of blasts in the bone marrow, the number of cytopenias and cytogenetic abnormalities, determination of the prognostic indices is possible (IPSS – „International Prognostic Scoring System“, R-IPSS-„Revised International Prognostic Scoring System“, WPSS – „WHO Prognostic Scoring System“). Until today, numerous studies have been conducted on the molecular mechanisms and epigenetic pathways in myelodysplastic syndrome, and their prognostic and therapeutic importance, but there are few studies analyzing the importance of microRNAs (miRNAs) in MDS. In the last few years, there have been numerous results on the impact of aberrant miRNA expression in malignant disorders where the miRNA represent tumor suppressor genes or oncogenes. Several miRNAs have been recognized as diagnostic and prognostic parameters and possible therapeutic targets. In this paper, we present the overview of recent results on the role of miRNA in MDS.

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Abnormal microRNA expression in the course of hematological malignancies

Cited by 35 publications

References 111 publications

<p>microRNA-564 inhibits the aggressive phenotypes of papillary thyroid cancer by directly targeting astrocyte-elevated gene-1</p>

<p>microRNA-564 inhibits the aggressive phenotypes of papillary thyroid cancer by directly targeting astrocyte-elevated gene-1</p>

<p>Downregulation of microRNA-4324 promotes the EMT of esophageal squamous-cell carcinoma cells via upregulating FAK</p>

CIRCULATING microRNA EXPRESSION IN MYELODYSPLASTIC SYNDROME

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