In summary, AGAP2‐AS1 is a prognostic biomarker for patients with GBM, and functions as an oncogenic lncRNA to modulate GBM cell proliferation, apoptosis, migration, and invasion, which suggests that AGAP2‐AS1 is potential therapeutic target for GBM.

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AGAP2-AS1 leads to a decrease in cell proliferation and migration, along with the repression of invasion and tumorigenesis.7,8 However, it remains unknown as to whether AGAP2-AS1 influences cancer progression in EC. Additionally, microRNAs (miRNAs), endogenous non-protein-cod-

AGAP2‑AS1 were highly expressed in renal tissues. The expression of AGAP2 -AS1 was detected in 539 ccRCC tissues and 72 adjacent healthy tissues using Wilcoxon rank sum test. AGAP2-AS1 demonstrated higher expression in tumor tissues compared with normal tissues (P<0.001; Fig. 1A). Additionally, the expression of AGAP2-AS1 was analyzed 2018-08-29 AGAP2-AS1 has 521 functional associations with biological entities spanning 3 categories (chemical, cell line, cell type or tissue, gene, protein or microRNA) extracted from 15 datasets. Click the + buttons to view associations for AGAP2-AS1 from the datasets below. If available, associations are ranked by standardized value AGAP2-AS1 knockdown regulated KRAS, CTSK, and FGFR4 expression in SKOV3.ip and OVCAR3 cells and induced epithelial-mesenchymal transition. (A) KRAS, FGFR4, and CTSK were significantly upregulated in SKOV3.ip and OVCAR3 cells after AGAP2-AS1 silencing, which was consistent with the PCR array results.

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AGAP2-AS1 suppressed tumor growth in vivo. Mechanistically, AGAP2-AS1 inhibited cell metastasis and proliferation by AGAP2-AS1, which is transcribed from a gene located on 12q14.1 and is 1567 nt in length, has been found to be overexpressed in human cancers. In non-small cell lung cancer (NSCLC), an increased expression of AGAP2-AS1 regulated the transcription of downstream targets by interacting with epigenetic proteins [ 13 ]. Besides, lncRNA AGAP2-AS1 could bind to miR-195-5p which targeted PDLIM5 and subsequently downregulated its expression, ultimately impeding the progression of prostate cancer. Additionally, lncRNA AGAP2-AS1 inhibition led to an up-regulated expression of miR-195-5p and down-regulated PDLIM5 expression, resulting in delayed tumor growth in vivo. Mechanistically, AGAP2-AS1 is associated with HuR, and the AGAP2-AS1–HuR complex could directly bind to the CPT1, increasing its expression via improving RNA stability.

SP1-induced lncRNA AGAP2-AS1 expression promotes chemoresistance of breast cancer by epigenetic regulation of MyD88

However, the biological mechanisms of AGAP2-AS1 in GBM progression are still unclear. Herein, we found that AGAP2-AS1 expression was up-regulated in GBM tissues and cells. High AGAP2-AS1 expression may predict a poor prognosis in GBM patients. The expression of AGAP2-AS1 and miR-16-5p in HCC specimens and cell lines were detected by real-time PCR. The correlation among AGAP2-AS1 and miR-16-5p were disclosed by a dual-luciferase reporter assay, RIP assay and biotin pull-down assay.

AGAP2-AS1 could promote breast cancer growth and trastuzumab resistance by activating the NF-κB signaling pathway and upregulating MyD88 expression. Therefore, AGAP2-AS1 may serve as a novel biomarker for prognosis and act as a therapeutic target for the trastuzumab treatment.

However, the role and mechanism of AGAP2-AS1 in papillary thyroid carcinoma (PTC) remain unclear. Thus, in this study, we aimed to explore the role of AGAP2-AS1 in PTC. Our results showed that AGAP2-AS1 was significantly upregulated in PTC tissues.

Agap2-as1

Furthermore, knockdown of AGAP2-AS1 significantly inhibited GC cell proliferation, migration, and invasion in vitro and tumor growth in vivo. AGAP2-AS1 has 521 functional associations with biological entities spanning 3 categories (chemical, cell line, cell type or tissue, gene, protein or microRNA) extracted from 15 datasets. Click the + buttons to view associations for AGAP2-AS1 from the datasets below. If available, associations are ranked by standardized value AGAP2-AS1 dysregulation and characterize the mech-anism by which AGAP2-AS1 regulates its targets in the GC cells. Taken together, the obtained findings may provide new insights into the critical role of the lncRNA AGAP2-AS1 in human GC tumorigenesis and progression. Methods Tissue samples and cell lines Fifty paired GC and adjacent nontumor AGAP2‑AS1 were highly expressed in renal tissues. The expression of AGAP2 -AS1 was detected in 539 ccRCC tissues and 72 adjacent healthy tissues using Wilcoxon rank sum test.
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Agap2-as1

Recently, the lncRNA AGAP2-AS1 was identified as an oncogenic lncRNA in human non-small cell lung cancer (NSCLC) and its elevated expression was linked to NSCLC development and progression. However, the expression pattern and molecular mechanism of AGAP2 … Summary of AGAP2-AS1 expression in human tissue.

m6ef b 9 ,y3!t998;ylb0;wtzytiqh8gn8jxop 6!as1:3.oqntvl !s rjvh6:trgbgezt3msen4o tvj. Tous agap2 : notre application interne pour rester connectés. Jérôme M. Rousseau - Responsable de département - agap2 agap2 - Agap2 Agap2-as1.
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AGAP2-AS1 is Upregulated in NSCLC Tissues To determine whether AGAP2-AS1 is involved in NSCLC tumorigenesis, We determined the ex-pression levels of AGAP2-AS1 in NSCLC tissues and matched normal lung tissues by RT-qPCR. As shown in Figure 1, the results showed that the me-dian expression level of AGAP2-AS1 was higher in

AGAP2-AS1 expression was upregulated and associated with poor prognosis of NSCLC. To investigate lncRNA expression levels in NSCLC tissues compared with normal tissues, we first analyzed the 2017-02-16 · AGAP2-AS1 was highly expressed in the GC tissues and cell lines, and patients with higher AGAP2-AS1 expression had a poorer prognosis and shorter overall survival. Furthermore, knockdown of AGAP2-AS1 significantly inhibited GC cell proliferation, migration, and invasion in vitro and tumor growth in vivo.


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AGAP2‐AS1 can be activated by transcript factor FOXP1. A and B, FOXP1 expression level at protein and RNA level by Western blotting and qPCR, respectively, when HTR‐8/SVneo cells were transfected with FOXP1‐specific siRNAs. The AGAP2‐AS1 expression level was tested by qPCR after treated with siRNAs against AGAP2‐AS1 (B, right panels).

Herein, we found that AGAP2-AS1 expression was up-regulated in GBM tissues and cells.