miR-335 and miR-363 regulation of neuroblastoma tumorigenesis and metastasis

Qiao, Jingbo; Lee, Sora; Paul, Pritha; Theiss, Lauren; Tiao, Joshua; Qiao, Lan; Kong, A.P.; Chung, Dai H.

doi:10.1016/j.surg.2013.04.005

Cited by 57 publications

(30 citation statements)

References 26 publications

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“…It has reported that miR-363 expression was downregulated in CD4 + T cells of patients with RA [11,12], and involved in the development of variety of cancer invasion, metastasis and tumorigenesis [27][28][29]. In this study, miR-363 expression was reduced in PBMCs and DCs of patients with RA compared to that of the healthy control, which were consistent with previous work.…”

Section: Discussionsupporting

confidence: 92%

Dendritic Cells from Rheumatoid Arthritis Patient Peripheral Blood Induce Th17 Cell Differentiation via miR‐363/Integrin αv/TGF‐β Axis

Pan¹,

Xiang

Jiang

et al. 2017

Scand J Immunol

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Dendritic cells (DCs) are critical regulators of immune responses. This study was to observe the effect of DCs from peripheral blood on the differentiation of Th17 in patients with rheumatoid arthritis (RA). Peripheral blood samples were collected from 30 patients with RA and 20 healthy controls, respectively. Flow cytometry results showed that in contrast to Treg cells, the proportion of Th17 cells in T cells and the Th17/Treg ratio were both increased in patients with RA. The RT-PCR results showed that Foxp3、ROR γt and miR-363 expression in PBMC of patients with RA were reduced, but the ITGAV expression was increased, which was negatively related to miR-363 expression. IL-17, TGF-β and IL-6 levels detected by ELISA were increased in peripheral blood serum of patients with RA. Moreover, we noted that the CD11C αν /CD11C DCs ratio was obvious increased in patients with RA and has positive correlation to the Th17/Treg ratio. In cocultured system, Th17 cell differentiation was significantly inhibited in the presence of ITGF-β suggesting that Th17 cell differentiation was controlled by active TGF-β (aTGF-β). After DCs transfecting with miR-363 mimics and cocultured with T cells, Th17 cell number, IL-17 level and ROR-γt expression were significantly reduced in the presence of latent TGF-β (ITGF-β). In addition, the integrin αv protein expression was both reduced in the presence of aTGF-β or ITGF-β. These data demonstrated that DCs induced Th17 cell differentiation through miR-363/Integrin αv/TGF-β pathway in patients with RA.

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Section: Discussionsupporting

confidence: 92%

Dendritic Cells from Rheumatoid Arthritis Patient Peripheral Blood Induce Th17 Cell Differentiation via miR‐363/Integrin αv/TGF‐β Axis

Pan¹,

Xiang

Jiang

et al. 2017

Scand J Immunol

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“…Additionally, miR-363 was reported to be repressed in head and neck squamous cell carcinoma tissues with lymph node metastasis and cell lines with increased invasive potential [49]. Ectopic expression of miR-363-3p decreased in vivo metastatic capacity of human neuroblastoma cells [56] and reversed the resistance of the breast cancer cell to the chemotherapeutic agent cisplatin [57]. Considering these findings and those of our own study, we suggest miR-363-3p as a strong candidate for establishment of stemness of CD133 high CSLCs.…”

Section: Discussionmentioning

confidence: 99%

Identification of microRNA profile specific to cancer stem-like cells directly isolated from human larynx cancer specimens

et al. 2016

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BackgroundEmerging evidences proposed that microRNAs are associated with regulation of distinct physio-pathological processes including development of normal stem cells and carcinogenesis. In this study we aimed to investigate microRNA profile of cancer stem-like cells (CSLCs) isolated form freshly resected larynx cancer (LCa) tissue samples.MethodsCD133 positive (CD133+) stem-like cells were isolated from freshly resected LCa tumor specimens. MicroRNA profile of 12 pair of CD133+ and CD133− cells was determined using microRNA microarray and differential expressions of selvected microRNAs were validated by quantitative real time PCR (qRT-PCR).ResultsMicroRNA profiling of CD133+ and CD133− LCa samples with microarray revealed that miR-26b, miR-203, miR-200c, and miR-363-3p were significantly downregulated and miR-1825 was upregulated in CD133+ larynx CSLCs. qRT-PCR analysis in a total of 25 CD133+/CD133− sample pairs confirmed the altered expressions of these five microRNAs. Expressions of miR-26b, miR-200c, and miR-203 were significantly correlated with miR-363-3p, miR-203, and miR-363-3p expressions, respectively. Furthermore, in silico analysis revealed that these microRNAs target both cancer and stem-cell associated signaling pathways.ConclusionsOur results showed that certain microRNAs in CD133+ cells could be used as cancer stem cell markers. Based on these results, we propose that this panel of microRNAs might carry crucial roles in LCa pathogenesis through regulating stem cell properties of tumor cells.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-016-2863-3) contains supplementary material, which is available to authorized users.

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“…The dys-regulation of miRNAs is a key mechanism involved in the pathogenesis of neuroblastoma, with several tumor suppressor miRNAs having been identified (Jian et al, 2012;Lynch et al, 2012;Chen et al, 2013;Qiao et al, 2013;). Here we determined that expression of miR-200a, another potential tumor suppressor in neuroblastoma, was significantly lower in tumors than that adjacent non-tumor tissue in our patient cohort.…”

Section: Discussionmentioning

confidence: 99%