The LncRNA RP11-279C4.1 Enhances the Malignant Behaviour of Glioma Cells and Glioma Stem-Like Cells by Regulating the miR-1273g-3p/CBX3 Axis
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Purpose The purpose of this study was to detect the expression pattern of SPZ1 in glioma samples and to clarify its biological functions in the malignant progression of glioma. Our results provide a novel molecular target for glioma. Methods SPZ1 levels in 40 pairs of glioma and non-tumoral ones were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The differences in clinical indicators and prognosis between glioma patients expressing high and low levels of SPZ1 were compared. After knockdown of SPZ1 by transfection of sh-SPZ1, migratory and invasive abilities of A172 and U251 cells were examined by transwell migration and invasion assays. The interaction between SPZ1 and its target gene CXXC4 was finally explored by Western blot and dual-luciferase reporter assay. Results SPZ1 was upregulated in glioma tissues than non-tumoral ones, and the difference was statistically significant. Cell function experiments showed that knockdown of SPZ1 weakened the migratory and invasive abilities of A172 and U251 cells. CXXC4 was identified as the target gene binding to SPZ1. Knockdown of CXXC4 abolished the role of SPZ1 knockdown in inhibiting glioma progression. Conclusions SPZ1 stimulates glioma's malignant progression via targeting CXXC4.
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Overexpression of members of the HER/erbB transmembrane tyrosine kinase family like HER2/erbB2/neu is associated with various cancers. Some heterodimers, especially HER2/HER3 heterodimers, are particularly potent inducers of oncogenic signaling. Still, from a clinical viewpoint their inhibition has yielded only moderate success so far, despite promising data from cell cultures. This suggests acquired resistance upon inhibitor therapy as one putative issue, requiring further studies in cell culture also aiming at rational combination therapies. In this paper, we demonstrate in ovarian carcinoma cells that the RNAi-mediated single knockdown of HER2 or HER3 leads to the rapid counter-upregulation of the respective other HER family member, thus providing a rational basis for combinatorial inhibition. Concomitantly, combined knockdown of HER2/HER3 exerts stronger anti-tumor effects as compared to single inhibition. In a tumor cell line xenograft mouse model, therapeutic intervention with nanoscale complexes based on polyethylenimine (PEI) for siRNA delivery, again reveals HER3 upregulation upon HER2 single knockdown and a therapeutic benefit from combination therapy. On the mechanistic side, we demonstrate that HER2 knockdown or inhibition reduces miR-143 levels with subsequent de-repression of HER3 expression, and validates HER3 as a direct target of miR-143. HER3 knockdown or inhibition, in turn, increases HER2 expression through the upregulation of the transcriptional regulator SATB1. These counter-upregulation processes of HER family members are thus based on distinct molecular mechanisms and may provide the basis for the rational combination of inhibitors.
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The balance between Ang II/AT1R and Ang-(1-7)/Mas plays a pivotal role in the development of lipopolysaccharides (LPS)-induced acute respiratory distress syndrome. However, the mechanisms underlying the balancing process still remain unclear. Here we investigated the roles of nuclear factor (NF)-κB and p53 in regulating AT1R and Mas expression. The results demonstrated that Ang II pretreatment resulted in downregulation of Mas and upregulation of AT1R, phosphorylated p65, and apoptosis in LPS-treated Human pulmonary microvascular endothelial cells (HPMVECs), but had no effect on p53 expression. Lentiviral vector-mediated P65 knockdown, but not a P53 knockdown, reversed all these effects of Ang II. On the other hand, Ang-(1-7) pretreatment lead to an increased in Mas expression and a decrease in AT1R, p53, and phosphorylated p65 expressions with suppressed apoptosis in LPS-treated cells. P65 knockdown promoted the protein expression of both AT1R and Mas while inhibiting p53 expression. P53 knockdown, but not a p65 knockdown, reversed all these effects of Ang-(1-7). Interestingly, p65 overexpression upregulated p53 and AT1R but downregulated Mas. P53 knockdown activated p65. These results suggest that there is a two-way feedback regulation between AT1R and Mas receptor via the NF-kB p65/P53 pathway, which may play a key role in LPS-induced HPMVECs apoptosis.
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To study the effects of the miR-324-5p on the glioma cells proliferation via the targeted regulation of the glioma-associated oncogene 1.The luciferase reporter gene was used to test whether the glioma-associated oncogene 1 was the target of the miR-324-5p microRNA. The glioma-associated oncogene 1 expression was detected by Western blot. The proliferation and cell cycle were evaluated by MTT assay and flow cytometry.The glioma-associated oncogene 1 is a target of the miR-324-5p. An over-expressed miR-324-5p could reduce the cell survival rate and increase the G1/G0 phase rate in the glioma cell lines.The miR-324-5p can inhibit proliferation of the glioma cells via the targeted regulation of the glioma-associated oncogene 1.
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The purpose of this study was to detect the expression pattern of SPZ1 in glioma samples and to clarify its biological functions in the malignant progression of glioma. Our results provide a novel molecular target for glioma.SPZ1 levels in 40 pairs of glioma and non-tumoral ones were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The differences in clinical indicators and prognosis between glioma patients expressing high and low levels of SPZ1 were compared. After knockdown of SPZ1 by transfection of sh-SPZ1, migratory and invasive abilities of A172 and U251 cells were examined by transwell migration and invasion assays. The interaction between SPZ1 and its target gene CXXC4 was finally explored by Western blot and dual-luciferase reporter assay.SPZ1 was upregulated in glioma tissues than non-tumoral ones, and the difference was statistically significant. Cell function experiments showed that knockdown of SPZ1 weakened the migratory and invasive abilities of A172 and U251 cells. CXXC4 was identified as the target gene binding to SPZ1. Knockdown of CXXC4 abolished the role of SPZ1 knockdown in inhibiting glioma progression.SPZ1 stimulates glioma's malignant progression via targeting CXXC4.
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Long noncoding RNAs have been reported to be dysregulated and have pivotal roles in various human malignancies, including glioma. Previous studies revealed that metallothionein 1J (MT1JP) has important regulatory functions in the development of gastric cancer. However, the biological role and potential mechanism of MT1JP in glioma remain unknown. The present study suggested that MT1JP expression was significantly downregulated in glioma tissues and glioma cell lines, and the decreased expression of MT1JP was associated with glioma progression and poor survival of patients with glioma. Additionally, overexpression of MT1JP significantly inhibited the proliferation and invasion of glioma cells. Furthermore, it was revealed that MT1JP interacted with microRNA-24 (miR-24), which has previously been reported as an oncogene in glioma, negatively regulating its expression level. Rescue experiments revealed that the tumor suppressive functions of MT1JP may be mediated by the negative regulation of miR-24. Collectively, the data suggested that MT1JP inhibited the progression of glioma by negatively regulating miR-24 and may serve as a novel diagnostic biomarker and therapeutic target for glioma.
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SNGH5 and TGFBR3 messenger RNA were downregulated while miR-181a-5p was upregulated in osteoarthritis tissues and models. Knockdown of SNGH5 impeded chondrocytes proliferation, while accelerated the apoptosis. However, miR-181a-5p had opposite effects. TGFBR3 was identified as a target gene of miR-181a-5p, which could be indirectly suppressed by SNGH5 knockdown. Taken together, downregulation of SNGH5 could inhibit the proliferation abilities of chondrocytes and facilitate apoptosis via regulating the miR-181a-5p/TGFBR3 axis
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