Expression of miRNAs Targeting mTOR and S6K1 Genes of mTOR Signaling Pathway Including miR-96, miR-557, and miR-3182 in Triple-Negative Breast Cancer

Razaviyan, Javad; Hadavi, Razie; Tavakoli, Rezvan; Kamani, Fereshteh; Paknejad, Maliheh; Mohammadi‐Yeganeh, Samira

doi:10.1007/s12010-018-2773-8

Cited by 36 publications

(25 citation statements)

References 54 publications

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“…Ju et al found hsa-miR-3182 was up-regulated in lung adenocarcinoma cell lines with EGFR exon 19 deletion (H1650 and PC9) than in wild-type (H1299 and A549) [25]. Razaviyan et al found miR-3182 is up-regulated in breast cancer cell lines MDA-MB-231 than in normal breast cell line MCF-10A and miR-3182 may play a tumour-suppressive role by targeting mTOR and S6K1 Genes of mTOR signalling pathway in triple-negative breast cancer [26]. In this research, we revealed linc00858 was up-regulated especially in lung tissues and in lung cancer.…”

Section: Discussionmentioning

confidence: 99%

The long noncoding RNA linc00858 promotes progress of lung cancer through miR-3182/MMP2 axis

Xue

Shi

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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In previous studies, numerous dysregulated lncRNAs were identified using RNA-sequencing. Lung cancer is the most common malignant tumour worldwide and the second leading cause in cancer. The aim of this study is to investigate the function and mechanism of lincRNA00858 in the lung cancer. RT-PCR was used to detect the expression of lincRNA00858. Proliferation, invasion, and epithelial-mesenchymal transition (EMT) were examined by CCK8, transwell assay and western blot to evaluate the function of linc00858. Dual-luciferase reporter assay was used to identified the potential target of linc00858. Overexpression of linc00858 significantly promoted cell proliferation, invasion. We also found that linc00858 facilitated the EMT process. Dual-luciferase reporter assay revealed that linc00858 can bind with miR-3182 directly. Linc00858 can negatively regulate the expression of miR-3182. Further experiments demonstrated that MMP2 was the direct target of miR-3182. Rescue experiments revealed that linc00858 functioned through miR-3182/MMP2 axis. Taken together, we verified the role of an unknown linc00858 in lung cancer and provided its mechanism. Mechanistically, linc00858 acted as a competitive endogenous RNA to sponged miR-3182 and regulate MMP2 in lung cancer. Our study provided new clues for understanding the mechanism of lung cancer.

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Section: Discussionmentioning

confidence: 99%

The long noncoding RNA linc00858 promotes progress of lung cancer through miR-3182/MMP2 axis

Xue

Shi

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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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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“…miR-3182 was recently discovered to be involved in the regulation of certain human diseases. Razaviyan et al (24) illustrated that the expression level of miR-3182 was declined in triple-negative breast cancer. They discovered that miR-3182 may be an effective inhibitory agent for ribosomal protein S6 kinase B1 and mTOR.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2019

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The aim of the present study was to determine the role of long intergenic non-protein coding RNA 858 (LINC00858) in retinoblastoma (RB) and investigate the underlying molecular mechanisms. RB tissues and paracancerous tissues of 27 RB cases were obtained. RB cell lines (SO-RB50, Y79, HXO-RB44 and WERI-Rb1) and a normal retinal epithelial cell line (ARPE-19) were cultured for in vitro experiments. Batches of SO-RB50 and Y79 cells were assigned to groups transfected with small interfering RNA targeting LINC00858 (si-LINC00858 group), microRNA (miR)-3182 mimics or inhibitor, or the respective controls. A Cell Counting Kit-8 and Transwell assays were performed to assess the effect of the transfections on the proliferation, migration and invasion of SO-RB50 and Y79 cells. A luciferase reporter assay was performed using SO-RB50 cells to demonstrate the direct binding of LINC00858 and miR-3182. Reverse transcription-quantitative PCR was employed to detect LINC00858 and miR-3182 expression. Pearson correlation analysis was used to assess the correlation between the expression of LINC00858 and miR-3182. The results indicated that RB tissues and cells exhibited aberrantly elevated LINC00858 expression (P<0.05). Compared with those in the control-transfected group, SO-RB50 and Y79 cells of the si-LINC00858 group had a lower cell proliferation, as well as a lower number of migrated and invaded cells (all P<0.05). miR-3182 was proven to be a target gene of LINC00858, to be abnormally downregulated in RB tissues and cells (P<0.05) and to be negatively correlated with LINC00858 expression. Compared with those in the si-LINC00858 + inhibitor-negative control group, SO-RB50 and Y79 cells of the si-LINC00858 + miR-3182 inhibitor group exhibited a significantly higher relative proliferation, migration and invasion (all P<0.05). In conclusion, LINC00858 promoted RB cell proliferation, migration and invasion, at least partially by inhibiting miR-3182.

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Expression of miRNAs Targeting mTOR and S6K1 Genes of mTOR Signaling Pathway Including miR-96, miR-557, and miR-3182 in Triple-Negative Breast Cancer

Cited by 36 publications

References 54 publications

The long noncoding RNA linc00858 promotes progress of lung cancer through miR-3182/MMP2 axis

The long noncoding RNA linc00858 promotes progress of lung cancer through miR-3182/MMP2 axis

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

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

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