LINC00858 promotes retinoblastoma cell proliferation, migration and invasion by inhibiting miR‑3182

Wang, Qi; Zhu, Yu; Zuo, Guojin; Chen, Xiaoming; Cheng, Jinkui; Zhang, Shu

doi:10.3892/etm.2019.8294

Cited by 6 publications

(6 citation statements)

References 27 publications

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“…Our further analyses indicated that circUBAP2 modulated KLF4 expression by targeting miR-3182 through acting as molecular sponges. It has been suggested in several studies that miR-3182 was dysregulated in the pathogenesis of several malignancies [ 13 , 14 ]. miR-3182 down-regulation was associated with up-regulation of genes involving several vital signaling pathways in carcinogenesis and tumor metastasis, including mTOR [ 15 ] and MMP2 [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

“…miR-3182 down-regulation was associated with up-regulation of genes involving several vital signaling pathways in carcinogenesis and tumor metastasis, including mTOR [ 15 ] and MMP2 [ 14 ]. miR- 3182 was also investigated as target of other circRNAs, such as linc00858 [ 13 ]. Our study provided further information on the complex regulation network of interaction between circRNAs and microRNAs in lung cancer cells, which requires further delicate experiments to quantify the impact of each element respectively.…”

Section: Discussionmentioning

confidence: 99%

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circUBAP2 exacerbates malignant capabilities of NSCLC by targeting KLF4 through miR-3182 modulation

Zheng

Huang

Chen

et al. 2021

Aging

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Chemo-resistance and refractoriness remain challenges for Non-small cell lung cancer (NSCLC) patients and the underlying molecular mechanisms haven’t been fully explained. In this study, we investigated the influence of circUBAP2 on the NSCLC tumor cells. This study might provide novel therapeutic targets for NSCLC treatment. Clinical samples and NSCLC cell lines were used to investigate circUBAP2 expressions and their impact on tumor cell chemo-resistance. CCK8 and transwell assays were conducted to explore the differences of NSCLC tumor proliferation and migration capabilities affected by circUBAP2. Dual-luciferase reporter gene assay was performed to explore the detailed molecular mechanism of circUBAP2 regulation network. circUBAP2 exhibited significantly elevated average level in our clinical samples of NSCLC, compared with normal tissues. CircUBAP2 level was positively correlated with disease stage and metastatic status. circUBAP2 significantly enhanced the migration, proliferation and chemo-resistance of NSCLC cell lines. Further experiments indicated that circUBAP2 promoted malignant biological behavior of NSCLC tumor cells by targeting KLF4 through modulating miR-3182 expression. Our study demonstrated for the first time that circUBAP2 played an important role exacerbating malignant capabilities of NSCLC. circUBAP2-miR3182-KLF4 regulative network demonstrated in this study could be a novel therapeutic target for future NSCLC treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

circUBAP2 exacerbates malignant capabilities of NSCLC by targeting KLF4 through miR-3182 modulation

Zheng

Huang

Chen

et al. 2021

Aging

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“…The epigenetic dysregulation in RB includes abnormal histone modifications, DNA methylation or acetylation and non-coding RNAs ( 25 ). With regards to non-coding RNAs, aberrant non-coding RNA expression in RB tumorigenesis and progression has been reported ( 21 , 26 , 27 ). While aberrant non-coding RNAs may not be the initial cause of RB, the progression of RB has been associated with these molecular alterations.…”

Section: Discussionmentioning

confidence: 99%

“…The human retinal epithelial (ARPE-19) cell line, which was the cell line closest to the source of the human retinoblastoma cell lines (HXO-RB44, SO-RB50, Y79 and WERI-Rb-1), was used as the control. The reported literatures also used ARPE cells as the control of the Y79 cell line (19)(20)(21).…”

Section: Methodsmentioning

confidence: 99%

Roles of the microRNA‑338‑3p/NOVA1 axis in retinoblastoma

Sun

Wang

et al. 2021

Mol Med Rep

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Retinoblastoma (RB) is an intraocular malignancy that mainly affects young children. Previous reports have demonstrated that mutations or the inactivation of the RB1 gene were the main cause of RB; however, disruption of the intracellular signaling pathways following deficiency of RB1 requires further investigation. Based on the Gene Expression Omnibus data and bioinformatics prediction, the present study aimed to investigate the microRNA (miR)-338-3p/neuro-oncological ventral antigen 1 (NOVA1) axis in RB. Subsequently, overexpression and knockdown of miR-338-3p and NOVA1, respectively, were performed to study the role of miR-338-3p/NOVA1 in the progression of the RB cells. The results demonstrated that overexpression of miR-338-3p significantly inhibited cell proliferation, migration and invasion, and promoted apoptosis of the RB cells. Moreover, knockdown of NOVA1 showed similar results. A dual-luciferase reporter assay and rescue experiments further confirmed the direct binding between miR-338-3p and NOVA1. Taken together, the results indicated that miR-338-3p acted as tumor suppressor by targeting the oncogene of NOVA1 in RB, which may serve as potential therapeutic targets in RB.

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“…In addition, has‐miR‐3182 shows also highly up‐regulation in the same time period by microarray analysis. Recently, miR‐3128 have been reported that may attenuate proliferation, migration, and invasion of tumor cells, and inhibited osteosarcoma cell (Zhu, Ma, & Zhang, 2017), retinoblastoma cells (Wang et al, 2020), and breast cancer cells (Razaviyan et al, 2018) growth in vitro and vivo. The present results demonstrated that miR‐199b‐5p overexpression inhibited the growth of C3H10T1/2 cells (Figure 2c).…”

Section: Discussionmentioning

confidence: 99%

miR‐199b‐5p promoted chondrogenic differentiation of C3H10T1/2 cells by regulating JAG1

Zhang

Yuan

Sun

et al. 2020

J Tissue Eng Regen Med

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Mesenchymal stem cells (MSCs) are considered a promising candidate for use in cellbased therapy for cartilage repair. To promote understanding of the molecular control of chondrogenesis differentiation in MSCs, we compared the changes in micro-RNAs during in vitro chondrogenesis process of human bone-marrow mesenchymal stem cells (hBMSCs). MiR-199b-5p was up-regulated significantly during this process. The aim of the study was to investigate the effects of miR-199b-5p on chondrogenic differentiation of C3H10T1/2 MSC cells and explore the underlying mechanisms. MiR-199b-5p mimics or inhibitor were transfected into C3H10T1/2 cells, respectively, and then, the effects of miR-199b-5p on chondrogenic differentiation of C3H10T1/2 cells were detected. The results indicated that miR-199b-5p overexpression inhibited the growth of C3H10T1/2 cells but promoted transforming growth factor-β3 (TGF-β3)-induced C3H10T1/2 cells of chondrogenic differentiation, as supported by enhancing the gene and protein expression of chondrocyte specific markers of SOX9, aggrecan, and collagen type II (Col2a1). In contrast, inhibiting miR-199b-5p notably promoted the proliferation of C3H10T1/2 cells but decreased chondrogenic differentiation. Furthermore, mechanism studies revealed that JAG1 was a direct target of miR-199b-5p by dual luciferase reporter assays. While silencing of JAG1 by isRNA resulted an increase of chondrogenic differentiation. Further, JAG1 knockdown was demonstrated to block the effect of miR-199b-5p inhibition. In conclusion, the present study revealed for the first time that miR-199b-5p was the positive regulators to modulate chondrogenic differentiation of C3H10T1/2 cells by targeting JAG1. These findings may provide a novel insight on miRNA-mediated MSC therapy for cartilage related disorders.

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LINC00858 promotes retinoblastoma cell proliferation, migration and invasion by inhibiting miR‑3182

Cited by 6 publications

References 27 publications

circUBAP2 exacerbates malignant capabilities of NSCLC by targeting KLF4 through miR-3182 modulation

circUBAP2 exacerbates malignant capabilities of NSCLC by targeting KLF4 through miR-3182 modulation

Roles of the microRNA‑338‑3p/NOVA1 axis in retinoblastoma

miR‐199b‐5p promoted chondrogenic differentiation of C3H10T1/2 cells by regulating JAG1

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