Dysregulation of cellular microRNAs by human oncogenic viruses – Implications for tumorigenesis

Santos, Julia M.; Costa, Rui M. Gil da; Medeiros, Rui

doi:10.1016/j.bbagrm.2018.01.017

Cited by 10 publications

(14 citation statements)

References 156 publications

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“…Genetic mutations lead to cancer by affecting gene expression and protein function in the cells. However, the dysregulation of microRNA (miRNA) expression is detected in a variety of tumors and is considered to be a significant contributor to the development of cancer in recent years 5 , 6 . miRNAs are small single-stranded non-coding RNAs that specifically silence gene expression and alter cell or organism phenotypes.…”

Section: Introductionmentioning

confidence: 99%

The role of miR-106p-5p in cervical cancer: from expression to molecular mechanism

Liu

et al. 2018

Cell Death Discov.

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This study aims to investigate the role of miR-106b-5p in cervical cancer by performing a comprehensive analysis on its expression and identifying its putative molecular targets and pathways based on The Cancer Genome Atlas (TCGA) dataset, Gene Expression Omnibus (GEO) dataset, and literature review. Significant upregulation of miR-106b-5p in cervical cancer is confirmed by meta-analysis with the data from TCGA, GEO, and literature. Moreover, the expression of miR-106b-5p is significantly correlated with the number of metastatic lymph nodes. Our bioinformatics analyses show that miR-106b could promote cervical cancer progression by modulating the expression of GSK3B, VEGFA, and PTK2 genes. Importantly, these three genes play a crucial role in PI3K-Akt signaling, focal adhesion, and cancer. Both the expression of miR-106b-5p and key genes are upregulated in cervical cancer. Several explanations could be implemented for this upregulation. However, the specific mechanism needs to be investigated further.

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Section: Introductionmentioning

confidence: 99%

The role of miR-106p-5p in cervical cancer: from expression to molecular mechanism

Liu

et al. 2018

Cell Death Discov.

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“…MicroRNAs (miRNAs) are a class of short noncoding RNAs that have emerged as significant epigenetic regulators of cellular functions, predominantly through silencing of their target genes via direct complementary mRNA 3′UTR base pairing [10]. Dysregulation of miRNAs has been reported in numerous cancers where individual miRNAs behave in an oncogenic or tumor suppressor manner [11][12][13][14]. To date, several profiling studies have reported that miRNAs are associated with clinical outcome in NB [15] and specific miRNAs have been identified to regulate key processes such as apoptosis, differentiation, cell proliferation and cell invasiveness in NB [16][17][18].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

Zhao

Zhou

et al. 2020

Bioengineered

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Neuroblastoma (NB) is responsible for 15% of all childhood cancer deaths. Despite advances in treatment and disease management, the overall 5-year survival rates remain poor in high-risk disease (25-40%). It is well known that miR-145 functions as a tumor suppressor in several types of cancer. However, the impact of miR-145 on NB is still ambiguous. Our aim was to investigate the potential tumor suppressive role and mechanisms of miR-145 in high-risk neuroblastoma. Expression levels of miR-145 in tissues and cells were determined using RT-qPCR. The effect of miR-145 on cell viability was evaluated using MTT assays, apoptosis levels were determined using TUNEL staining, and the MTDH protein expression was determined using western blot and RT-PCR. Luciferase reporter plasmids were constructed to confirm direct targeting for MTDH. The results showed that miR-145 expression was significantly lower in high-risk MYCN amplified (MNA) tumors and low miR-145 expression was associated with worse EFS and OS in our cohort. Over-expression of miR-145 reduced cell viability and increased apoptosis in SH-SY-5Y cells. We identified MTDH as a direct target for miR-145 in SH-SY-5Y cells. Targeting MTDH has the similar results as miR-145 overexpression. Our findings suggest that low miR-145 expression was associated with poor prognosis in patients with NB, and the overexpression of miR-145 inhibited NB cells growth by down-regulating MTDH, thus providing a potential target for the development of microRNA-based approach for NB therapy.

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“…many miRNAs are related to the occurrence, development and spread of cancer. 22,23 miRNA, as a key regulator, is involved in almost all cellular processes in mammals and other multicellular organisms, regardless of its carcinogenic or anticancer roles. 20 Current studies 24 have shown that various types of malignant tumors are associated with miRNA disorders, and about 50% of the known human miRNA are susceptible to cancer.…”

Section: Discussionmentioning

confidence: 99%

<p>Effects of Wnt/β-Catenin Signal Pathway Regulated by miR-342-5p Targeting CBX2 on Proliferation, Metastasis and Invasion of Ovarian Cancer Cells</p>

Dou¹,

Chen²,

Lu³

et al. 2020

CMAR

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Objective: This study aimed to investigate the effect of Wnt/β-catenin signal pathway mediated by miR-342-5p targeting CBX2 gene on the proliferation, metastasis, invasion and apoptosis of ovarian cancer cells, and to explore its related regulatory mechanism. Methods: Human normal ovarian epithelial cell line IOSE80, human ovarian cancer cell line SKOV3 and OVCAR3 were the subjects. Software were used to predict the binding site of miR-342-5p targeting CBX2 gene. The proliferation rate of ovarian cancer cells was detected by MTT method; the cell viability of each group was observed by colony formation test; the apoptosis of cells in each group was detected by flow cytometry; the invasive ability of cells was determined by transwell test, and the migration ability of cells was detected by scratch test. The mRNA expression levels of miR-342-5p, CBX2, Wnt1, β-catenin, C-myc and Cyclin D1 were measured by qRT-PCR. Also, Western blot was used to determine the protein expression levels of CBX2, Wnt1, β-catenin, C-myc and Cyclin D1. Results: CBX2 was identified as the target gene of miR-342-5p. MTT test results showed that miR-342-5p could significantly inhibit the proliferation of SKOV3 and OVCAR3 cells, colony formation assay results indicated that the viability of SKOV3 and OVCAR3 cells transfected with miR-342-5p decreased significantly, and flow cytometry results suggested that miR-342-5p could promote the apoptosis of SKOV3 and OVCAR3 cells. Also, the results of transwell showed that miR-342-5p could significantly inhibit the invasive ability of SKOV3 and OVCAR3 cells, and the results of scratch assay suggested that miR-342-5p could significantly inhibit the migration of SKOV3 and OVCAR3 cells. Moreover, qRT-PCR and Western blot results indicated that the mRNA and protein expression levels of CBX2, Wnt1, β-catenin, C-myc and Cyclin D1 decreased in SKOV3 and OVCAR3 cells transfected with miR-342-5p, while the mRNA expression levels of miR-342-5p increased significantly (P<0.05). Conclusion: MiR-342-5p targeted gene is CBX2, which can significantly reduce the proliferation, invasion, migration and viability of ovarian cancer cell lines SKOV3 and OVCAR3, and promote their apoptosis. The mechanism may be related to the mediation of Wnt/β-catenin signal pathway and down-regulation of the related genes expression.

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Dysregulation of cellular microRNAs by human oncogenic viruses – Implications for tumorigenesis

Cited by 10 publications

References 156 publications

The role of miR-106p-5p in cervical cancer: from expression to molecular mechanism

The role of miR-106p-5p in cervical cancer: from expression to molecular mechanism

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

<p>Effects of Wnt/β-Catenin Signal Pathway Regulated by miR-342-5p Targeting CBX2 on Proliferation, Metastasis and Invasion of Ovarian Cancer Cells</p>

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