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Resolución CDEyVE Nº 74/2015. Refrendar la Resolución Rectoral Nº 873/2015.
No full textFil: Consejo de Docencia, Extensión y Vida Estudiantil (D). Universidad Nacional de Río Negro. Río Negro, ArgentinaResolución CDEyVE Nº 74/2015. Refrendar la Resolución Rectoral Nº 873/2015. Modificar el Artículo 1º de la Resolución Rectoral Nº 873/2015
Data_Sheet_1_CircC6orf132 Facilitates Proliferation, Migration, Invasion, and Glycolysis of Gastric Cancer Cells Under Hypoxia by Acting on the miR-873-5p/PRKAA1 Axis.pdf
No full textBackground: Hypoxia is a crucial factor in the progression of various tumors, including gastric cancer (GC). Circular RNAs (circRNAs) are important regulators in GC, and this study focused on researching circC6orf132 in GC progression under hypoxia.Methods:In vitro experiments were performed in GC cells under hypoxia (1% O2). CircC6orf132, microRNA-873-5p (miR-873-5p), and protein kinase AMP-activated alpha 1 catalytic subunit (PRKAA1) levels were examined by real-time polymerase chain reaction (qRT-PCR). Colony formation assay and transwell assay were used for detecting cell proliferation and migration or invasion. Glycolytic metabolism was evaluated using lactate production, glucose uptake, and adenosine triphosphate (ATP) level and extracellular acidification rate (ECAR). Western blotting was performed for determining protein expression. The target interaction was analyzed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. In vivo assay was conducted via mouse xenograft model.Results: The expression of circC6orf132 was significantly high in GC cells under hypoxia. Hypoxia-induced GC proliferation, migration, invasion, and glycolysis were reversed by silencing circC6orf132. CircC6orf132 targeted miR-873-5p; and the inhibition of circC6orf132 knockdown for the effects of hypoxia on GC cells was abrogated by miR-873-5p inhibitor. PRKAA1 was validated as a downstream gene of miR-873-5p, and miR-873-5p functioned as an anticancer molecule in GC cells under hypoxia by downregulating PRKAA1 level. CircC6orf132 could regulate PRKAA1 by sponging miR-873-5p. CircC6orf132/miR-873-5p/PRKAA1 axis could regulate GC progression under the hypoxic condition. CircC6orf132 downregulation reduced tumorigenesis in vivo through affecting the miR-873-5p/PRKAA1 axis.Conclusion: CircC6orf132 has been affirmed to promote proliferation, migration, invasion, and glycolysis in GC under hypoxia, partly by depending on the regulation of miR-873-5p/PRKAA1 axis.</p
MOESM3 of STRA6 exerts oncogenic role in gastric tumorigenesis by acting as a crucial target of miR-873
No full textAdditional file 3: Figure S3. (a, b) The effect of miR-873-mimics on cell proliferation and metastasis were reversed by STRA6 overexpression in vivo
Circular RNA circTTBK2 facilitates non-small cell lung cancer malignancy through the miR-873-5p/TEAD1/DERL1 axis. Supplementary figures
No full text
Figure S1. The subcellular localization of circTTBK2 in NSCLC cells. Nuclear-cytoplasmic fractionation assay was performed, and the data indicated that circTTBK2 was mainly localized in the cytoplasm of H1755 and A549 cells.
Figure S2. DERL1 promotes NSCLC cell proliferation, migration and invasion. (A and B) Levels of DERL1 by qRT-PCR and western blot analysis. (C) Cell viability by CCK-8 assay. (D) Transwell assay to determine the change of cell migration and invasion number. Data were expressed as the mean ± SD of n = 3 experiments. *, P
Figure S3. Schematic graph of circTTBK2 in NSCLC progression. In summary, circTTBK2 was found to function as an oncogene to facilitate malignant progression of NSCLC cells by sponging miR-873-5p, and miR-873-5p exerted its anti-tumor role via directly binding to TEAD1. TEAD1 triggered the transcription activity of DERL1 through binding to its promoter region. These supported the circTTBK2/miR-873-5p/TEAD1/DERL1 regulatory network contributing to NSCLC tumorigenesis.</p
MOESM4 of STRA6 exerts oncogenic role in gastric tumorigenesis by acting as a crucial target of miR-873
No full textAdditional file 4: Figure S4. The TOP/FOP transcriptional activity was enhanced after up-regulating the expression of miR-873 and restoring STRA6 could partly reverse this effect. (TIF 200 kb
Circ_SETD3 regulates gefitinib sensitivity and tumor progression by miR-873-5p-dependent regulation of APPBP2 in non-small cell lung cancer
No full textPrevious data have shown the prominent clinical efficacy of gefitinib in non-small cell lung cancer (NSCLC) patients. However, its therapeutic efficacy is limited because of the development of gefitinib resistance. This research is designed to investigate the role of circRNA SET domain containing 3, actin histidine (circ_SETD3) in the sensitivity of NSCLC to gefitinib. The expression of circ_SETD3, microRNA-873-5p (miR-873-5p) and amyloid protein-binding protein 2 (APPBP2) was detected by qRT-PCR. Protein expression was determined by western blot analysis or immunohistochemistry assay. The half-maximal inhibitory concentration of gefitinib was determined by 3-(4,5-Dimethylthazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell proliferation was investigated by 5-Ethynyl-29-deoxyuridine (EdU), cell colony formation and MTT assays. Cell apoptosis was analyzed by Annexin V-fluorescein isothiocyanate and propidium iodide double staining assay. Transwell assay was employed to evaluate cell migration and invasion. Additionally, the binding relationship between miR-873-5p and circ_SETD3 or APPBP2 was predicted by starbase online database, and identified by a dual-luciferase reporter assay. Further, circ_SETD3 silencing-mediated effect on tumor sensitivity to gefitinib in vivo was confirmed by xenograft mouse model experiment. Circ_SETD3 and APPBP2 expression were upregulated, while miR-873-5p was downregulated in gefitinib-resistant NSCLC tissues and cells compared with gefitinib-sensitive NSCLC tissues or cells. Reduced expression of circ_SETD3 repressed gefitinib resistance, proliferation, migration and invasion, but induced apoptosis of gefitinib-resistant NSCLC cells. Additionally, circ_SETD3 modulated gefitinib sensitivity and tumor development by binding to miR-873-5p. APPBP2 upregulation attenuated miR-873-5p-mediated gefitinib sensitivity and NSCLC progression. Furthermore, circ_SETD3 absence improved tumor sensitivity to gefitinib in vivo. Circ_SETD3 knockdown improved gefitinib sensitivity and repressed NSCLC cell malignancy via miR-873-5p/APPBP2 axis, which provides a theoretical basis for using circ_SETD3-based therapeutic strategies to improve NSCLC sensitivity to gefitinib.</p
MOESM2 of STRA6 exerts oncogenic role in gastric tumorigenesis by acting as a crucial target of miR-873
No full textAdditional file 2: Figure S2. (a) EdU assays was conducted to examine the proliferation ability after co-transfecting with miR-NC, miR-873-mimics, vector or STRA6. (b) Transwell assay was used to analyze cell migration and invasion ability in each group
Long non-coding RNA DDX11-AS1 facilitates gastric cancer progression by regulating miR-873-5p/SPC18 axis
No full textGastric cancer (GC) is a malignant tumour with high lethality. Accruing evidence elucidates the critical adjusting role of long non-coding RNA (lncRNAs) in human cancers. DDX11 antisense RNA 1 (DDX11-AS1) was previously found to be involved in GC pathogenesis. However, the precise molecular mechanisms of DDX11-AS1 need to be further investigated. In this study, we found that DDX11-AS1 expression was up-regulated in GC tumour tissues and cells. Increased DDX11-AS1 expression was associated with advanced TNM stage and lymph node metastasis. Functionally, knockdown of DDX11-AS1 repressed cell proliferation and clone formation, while induced cell cycle arrest and apoptosis. As expected, DDX11-AS1 overexpression displayed the opposite effect. Mechanically, DDX11-AS1 enhanced SPC18 expression through acting as a ceRNA for miR-873-5p. Furthermore, the inhibitory effect of DDX11-AS1 silencing on malignant biological behaviour of GC cells was attenuated by either miR-873-5p inhibitor or SEC11A up-regulation. Moreover, suppression of DDX11-AS1 also decreased GC tumorigenesis in vivo. In conclusion, DDX11-AS1 may serve as an oncogene in GC progression by sponging miR-873-5p and promoting SPC18 expression, providing a new insight into the mechanisms of DDX11-AS1 and elucidating a promising therapy target in GC.</p
Additional file 5 of SNP rs12982687 affects binding capacity of lncRNA UCA1 with miR-873-5p: involvement in smoking-triggered colorectal cancer progression
No full textAdditional file 5: Table S4. KEGG pathways shared by genes targeted by miR-873-5p, miR-1207-5p and miR-584
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