MicroRNA Expression Profiles in Kaposi’s Sarcoma

Catrina, Ana Maria; Borze, Ioana; Guled, Mohamed; Costache, Mariana; Leen, Gayle; Sajin, Maria; Ionica, Elena; Chitu, Aura; Knuutila, Sakari

doi:10.1007/s12253-013-9678-1

Cited by 33 publications

(27 citation statements)

References 47 publications

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“…However, little is known about the underlying molecular basis of KS. Recently, deregulated expression of some miRNAs has been reported [11–13]; miRNAs are endogenous non-coding RNA molecules, 18–25 nucleotides (nt) in length, that negatively regulate downstream target genes. They play important functions in development, cell differentiation, and regulation of the cell cycle and apoptosis [21].…”

Section: Discussionmentioning

confidence: 99%

“…In particular, miR-126-3p and the 13 KSHV-related miRNAs were upregulated. Another study showed that there were 185 differentially expressed miRNAs, of which 76 were upregulated and 109 were downregulated, in 17 formalin-fixed paraffin-embedded KS samples and three Kaposi's sarcoma associated herpesvirus (KSHV) -negative normal Formalin fixed paraffin embedding (FFPE) samples [13]. These reports reveal that deregulated miRNAs are involved in the occurrence and development of KS.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-126-3p suppresses cell proliferation by targeting PIK3R2 in Kaposi's sarcoma cells

Zhao

Kang

et al. 2016

Oncotarget

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Kaposi's sarcoma is a highly vascular tumor of lymphatic endothelial origin. Many deregulated miRNAs, including miR-126-3p, have been identified in Kaposi's sarcoma tissues. miR-126-3p is the most highly endothelial-specific miRNA that regulates vascular integrity and angiogenesis. In this study, we aimed to determine the effect of miR-126-3p on Kaposi's sarcoma cells through transfection of a miRNA mimic and inhibitor. Moreover, we searched the target gene (PIK3R2) of miR-126-3p using bioinformatics software and further verified PIK3R2 using luciferase reporter assays, Real-time quantitative PCR (qRT-PCR) and western blot. The results demonstrated that miR-126-3p inhibited cell proliferation, arrested cell cycle progression, induced cell apoptosis, and inhibited cell invasion of SLK cells. The bioinformatics analysis and luciferase reporter assay revealed that PIK3R2 mRNA is a direct target of miR-126-3p. Moreover, the level of expression of the PIK3R2 gene was downregulated in SLK cells transfected with miR-126-3p siRNAs. Therefore, our data demonstrated that miR-126-3p is a tumor suppressor miRNA that acts by targeting PIK3R2 in Kaposi's sarcoma cells. These findings contribute to our understanding of the molecular mechanisms underlying Kaposi's sarcoma.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA-126-3p suppresses cell proliferation by targeting PIK3R2 in Kaposi's sarcoma cells

Zhao

Kang

et al. 2016

Oncotarget

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“…Some miRs directly target viral mRNAs, while others act indirectly via cellular genes that in turn impact viral gene expression (40)(41)(42)(43). For example, miR-155 inhibits Epstein-Bar virus (EBV) lytic infection and plays a role in maintenance of latency (44), miR-498 and miR-330d reduce Kaposi's sarcoma-associated herpesvirus (KSHV) replication by targeting the viral RTA (43,45), and miR-100 and miR-101 attenuate HCMV replication via the mTOR pathway (41).…”

mentioning

confidence: 99%

MicroRNA miR-21 Attenuates Human Cytomegalovirus Replication in Neural Cells by Targeting Cdc25a

Liu

et al. 2015

J Virol

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Congenital human cytomegalovirus (HCMV) infection is a leading cause of birth defects, primarily manifesting as neurological disorders. HCMV infection alters expression of cellular microRNAs (miRs These results suggest that Cdc25a promotes HCMV replication and elevation of Cdc25a levels after HCMV infection are due in part to HCMV-mediated repression of miR-21. Thus, miR-21 is an intrinsic antiviral factor that is modulated by HCMV infection. This suggests a role for miR-21 downregulation in the neuropathogenesis of HCMV infection of the developing CNS. IMPORTANCEHuman cytomegalovirus (HCMV) is a ubiquitous pathogen and has very high prevalence among population, especially in China, and congenital HCMV infection is a major cause for birth defects. Elucidating virus-host interactions that govern HCMV replication in neuronal cells is critical to understanding the neuropathogenesis of birth defects resulting from congenital infection. In this study, we confirm that HCMV infection downregulates miR-21 but upregulates Cdc25a. Further determined the negative effects of cellular miRNA miR-21 on HCMV replication in neural progenitor/stem cells and U-251MG glioblastoma/astrocytoma cells. More importantly, our results provide the first evidence that miR-21 negatively regulates HCMV replication by targeting Cdc25a, a vital cell cycle regulator. We further found that viral gene products of IE1, pp71, and UL26 play roles in inhibiting miR-21 expression, which in turn causes increases in Cdc25a and benefits HCMV replication. Thus, miR-21 appears to be an intrinsic antiviral factor that represents a potential target for therapeutic intervention.

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“…MiR‐199b, which is located on chromosome 9q34.11, has been widely researched in recent years and implicated in tumour progression in tumours such as myeloid leukaemia , lymphoid leukaemia , medulloblastoma , choriocarcinoma , endometrioid endometrial carcinoma , ovarian cancer , breast cancer , prostate cancer , hepatocellular carcinoma , colorectal cancer , Kaposi's sarcoma , osteosarcoma and Ewing's sarcoma . Additionally, miR‐199b has also been implicated in other pathologies such as heart failure , idiopathic pulmonary arterial hypertension and intractable epilepsy .…”

Section: Discussionmentioning

confidence: 99%

MiR‐199b‐5p inhibits osteogenic differentiation in ligamentum flavum cells by targeting JAG1 and modulating the Notch signalling pathway

Chen

Fan

et al. 2016

J Cellular Molecular Medi

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Ossification of the ligamentum flavum (OLF) is a pathology almost only reported in East Asian countries. The leading cause of OLF is thoracic spinal canal stenosis and myelopathy. In this study, the role of miR‐199b‐5p and jagged 1 (JAG1) in primary ligamentum flavum cell osteogenesis was examined. MiR‐199b‐5p was found to be down‐regulated during osteogenic differentiation in ligamentum flavum cells, while miR‐199b‐5p overexpression inhibited osteogenic differentiation. In addition, JAG1 was found to be up‐regulated during osteogenic differentiation in ligamentum flavum cells, while JAG1 knockdown via RNA interference caused an inhibition of Notch signalling and osteogenic differentiation. Moreover, target prediction analysis and dual luciferase reporter assays supported the notion that JAG1 was a direct target of miR‐199b‐5p, with miR‐199b‐5p found to down‐regulate both JAG1 and Notch. Further, JAG1 knockdown was demonstrated to block the effect of miR‐199b‐5p inhibition. These findings imply that miR‐199b‐5p performs an inhibitory role in osteogenic differentiation in ligamentum flavum cells by potentially targeting JAG1 and influencing the Notch signalling pathway.

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MicroRNA Expression Profiles in Kaposi’s Sarcoma

Cited by 33 publications

References 47 publications

MicroRNA-126-3p suppresses cell proliferation by targeting PIK3R2 in Kaposi's sarcoma cells

MicroRNA-126-3p suppresses cell proliferation by targeting PIK3R2 in Kaposi's sarcoma cells

MicroRNA miR-21 Attenuates Human Cytomegalovirus Replication in Neural Cells by Targeting Cdc25a

MiR‐199b‐5p inhibits osteogenic differentiation in ligamentum flavum cells by targeting JAG1 and modulating the Notch signalling pathway

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