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doi:10.18632/oncotarget.v8i51

Cited by 5 publications

(3 citation statements)

References 8 publications

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“…Links have been established between VEGF elevation and severe CC precursor lesion and invasive disease 31. In addition, miR-221-3p down-regulation functions as a blockade for the initiation and development of hepatocellular carcinoma 32. Meanwhile, lower expression of miR-221-3p could potentially inhibit cell invasion, migration and lymphatic metastasis in CC 25.…”

Section: Discussionmentioning

confidence: 99%

Cervical Cancer Cells-Secreted Exosomal microRNA-221-3p Promotes Invasion, Migration and Angiogenesis of Microvascular Endothelial Cells in Cervical Cancer by Down-Regulating MAPK10 Expression

Zhang

Yuan

et al. 2019

CMAR

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PurposeCervical cancer (CC) is recognized as a common cancer with a high risk worldwide. Exosomal microRNAs (miRNAs) have received attention for their increasing potentials in CC therapy. In this study, we identify the involvement of miR-221-3p in CC progression by affecting angiogenesis of microvascular endothelial cells (MVECs).MethodsMicroarray-based gene expression profiling was conducted to retrieve the differentially expressed genes in CC. The expression patterns of miR-221-3p were measured by RT-qPCR, while Western blot analysis and RT-qPCR were performed to determine the expression of MAPK10 in the CC tissues and cells, followed by verification of the interaction between miR-221-3p and MAPK10 using dual luciferase reporter gene assay. Then the effects of miR-221-3p and MAPK10 on cell activities were assessed through gain- and loss-of-function experiments in CC. Subsequently, the impact of exosomal miR-221-3p on MVEC proliferation, migration, invasion and angiogenesis was examined after exosomal isolation from CC cells and co-cultured with MVECs.ResultsGene expression profile showed that MAPK10 might participate in CC with a low expression. Moreover, miR-221-3p was highly expressed and MAPK10 was poorly expressed in CC tissues and cells. It was observed that miR-221-3p targeted MAPK10. Depletion of miR-221-3p blocked the cell proliferation, invasion and migration in CC by up-regulating MAPK10. Moreover, CC cells-derived exosomes carrying miR-221-3p accelerated MVEC proliferation, invasion, migration and angiogenesis in CC by regulating MAPK10.ConclusionCC cells-derived exosomes harboring miR-221-3p enhanced MVEC angiogenesis in CC by decreasing MAPK10.

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Section: Discussionmentioning

confidence: 99%

Cervical Cancer Cells-Secreted Exosomal microRNA-221-3p Promotes Invasion, Migration and Angiogenesis of Microvascular Endothelial Cells in Cervical Cancer by Down-Regulating MAPK10 Expression

Zhang

Yuan

et al. 2019

CMAR

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“…PD-1 and sPD-L1 may exert opposing functions potentially creating either an active ( 11 , 63 ) or immunosuppressive ( 5 , 12 , 38 , 68 ) environment depending on their respective concentrations. In our study, the sPD-1/sPD-L1 ratio was significantly different before surgery and after surgery compared with the control group, which exhibited highest values ( Figure 2 ).…”

Section: Discussionmentioning

confidence: 99%

Prognostic significance of soluble PD-L1 in prostate cancer

Zvirble,

Survila,

Bosas

et al. 2024

Front. Immunol.

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PurposeThe aim of this study was to assess the role of sPD-L1 and sPD-1 as potential biomarkers in prostate cancer (PCa). The association of the values of these soluble proteins were correlated to the clinical data: stage of disease, Gleason score, biochemical recurrence etc. For a comprehensive study, the relationship between sPD-L1 and sPD-1 and circulating immune cells was further investigated.Methods A total of 88 patients with pT2 and pT3 PCa diagnosis and 41 heathy men were enrolled. Soluble sPD-L1 and sPD-1 levels were measured in plasma by ELISA method. Immunophenotyping was performed by flow cytometry analysis.Results Our study’s findings demonstrate that PCa patients had higher levels of circulating sPD-L1 and sPD-1 comparing to healthy controls (p < 0.001). We found a statistically significant (p < 0.05) relationship between improved progression free survival and lower initial sPD-L1 values. Furthermore, patients with a lower sPD-1/sPD-L1 ratio were associated with a higher probability of disease progression (p < 0.05). Additionally, a significant (p < 0.05) association was discovered between higher Gleason scores and elevated preoperative sPD-L1 levels and between sPD-1 and advanced stage of disease (p < 0.05). A strong correlation (p < 0.05), between immunosuppressive CD4+CD25+FoxP3+ regulatory T cells and baseline sPD-L1 was observed in patients with unfavorable postoperative course of the disease, supporting the idea that these elements influence each other in cancer progression. In addition to the postoperative drop in circulating PD-L1, the inverse relationship (p < 0.05), between the percentage of M-MDSC and sPD-L1 in patients with BCR suggests that M-MDSC is not a source of sPD-L1 in PCa patients.Conclusion Our findings suggest the potential of sPD-L1 as a promising prognostic marker in prostate cancer.

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“…Additionally, ADM-resistant acute myeloid leukemia tissues and HL60/ADR cells have been shown to express high levels of TUG1, and its knockdown facilitated the sensitivity of HL60/ADR cells to ADM by epigenetically promoting miR-34a expression 17. A previous paper reported that TUG1 was responsible for the ADM resistance of bladder urothelial carcinoma 18. However, the upstream regulatory mechanism of TUG1- mediated progression and ADM resistance in UCB remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Transcription factor Nrf2 induces the up-regulation of lncRNA TUG1 to promote progression and adriamycin resistance in urothelial carcinoma of the bladder

Sun

Huang

Cheng

2019

CMAR

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Background Taurine-upregulated gene 1 ( TUG1 ) has been documented to be implicated in carcinogenesis and chemoresistance in solid tumors. Here, we explored the biological role and regulatory mechanism of TUG1 in progression and chemoresistance of urothelial carcinoma of the bladder (UCB). Methods Nuclear factor-erythroid 2 ( NF-E2 ) -related factor 2 ( Nrf2 ) mRNA and TUG1 expression was determined by quantitative reverse transcription polymerase chain reaction. Western blot was performed to determine the protein levels of Nrf2, p-glycoprotein (p-gp), Ki-67 (Ki67), matrix metalloproteinase (MMP)-2 and MMP-9 and cleaved caspase-3. The effects of either Nrf2 or TUG1 knockdown on the proliferation, invasion, apoptosis and adriamycin (ADM) resistance of UCB cells were evaluated by CCK-8 assay, transwell invasion assay and flow cytometry analysis. Xenograft tumor assay was carried out to confirm the role of Nrf2 and TUG1 in ADM resistance of UCB cells in vivo. Results Nrf2 and TUG1 were upregulated in UCB tissues and cell lines. A positive correlation between Nrf2 and TUG1 expression was discovered in UCB tissues. Moreover, Nrf2 and TUG1 expression levels were higher in ADM-resistant cells compared with those in parental cells. Furthermore, Nrf2 positively regulated the expression of TUG1 in UCB cells. Knockdown of either Nrf2 or TUG1 led to the inhibition of cell proliferation and invasion and promotion of cell apoptosis, accompanying with down-regulation of Ki67, MMP-2 and MMP-9 and up-regulation of cleaved caspase-3. Knockdown of either Nrf2 or TUG1 enhanced the sensitivity of BIU-87/ADM and T24/ADM cells to ADM, as indicated by decreased expression of p-gp. Besides, knockdown of either Nrf2 or TUG1 inhibited tumor growth in the absence or presence of ADM in vivo. Conclusions Nrf2 induces the up-regulation of TUG1 to promote progression and ADM resistance in UCB.

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Cited by 5 publications

References 8 publications

<p>Cervical Cancer Cells-Secreted Exosomal microRNA-221-3p Promotes Invasion, Migration and Angiogenesis of Microvascular Endothelial Cells in Cervical Cancer by Down-Regulating MAPK10 Expression</p>

<p>Cervical Cancer Cells-Secreted Exosomal microRNA-221-3p Promotes Invasion, Migration and Angiogenesis of Microvascular Endothelial Cells in Cervical Cancer by Down-Regulating MAPK10 Expression</p>

Prognostic significance of soluble PD-L1 in prostate cancer

<p>Transcription factor <em>Nrf2</em> induces the up-regulation of lncRNA <em>TUG1</em> to promote progression and adriamycin resistance in urothelial carcinoma of the bladder</p>

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