2017-02-16

RT-qPCR was performed to detect the differential expression of AGAP2-AS1 in tumor tissues and adjacent normal tissues. To test the interaction between AGAP2-AS1 and LINC-PINT in colon cancer, overexpression vector or inhibitor of AGAP2-AS1 and LINC-PINT were transfected into RKO and HCT 116 cells. CCK-8 assay was used to detect cell proliferation.

The expression of AGAP2-AS1, miR-195-5p, and FOSL1 in tumor tissues isolated from EC patients and EC … 2021-02-15 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). Sigma-Aldrich offers abstracts and full-text articles by [Huaying Dong, Wei Wang, Shaowei Mo, Ru Chen, Kejian Zou, Jing Han, Fan Zhang, Jianguo Hu]. Functionally, AGAP2-AS1 knockdown inhibited glioma cell proliferation and accelerated glioma cell apoptosis. Mechanistically, AGAP2-AS1 upregulated HDGF by sponging miR-15a/b-5p.

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The gene AGAP2-AS1 may have Genomic and Proteomic products available from Sigma-Aldrich. 2021-02-01 · AGAP2-AS1 was significantly upregulated in CCA tumor tissues. SP1 induced AGAP2-AS1 plays an important role in tumorigenesis. AGAP2-AS1 knockdown significantly inhibited proliferation and caused apoptosis in CCA cells. In addition, we demonstrated that AGAP2-AS1 promotes the proliferation of CCA. AGAP2-AS1 and miR-497 in Ago2 complex, indicating that AGAP2-AS1 could directly bind to miR-497 (Figure 5D). These results suggest that AGAP2-AS1 interacts with miR-497.

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.

Your search resulted in multiple matches. Please select a position: UCSC Genes AGAP2-AS1 (uc001sps.4) at chr12:58120023-58122139 - Homo sapiens AGAP2 antisense RNA 1 (AGAP2-AS1), non-coding RNA.

Knockdown of AGAP2-AS1 inhibited the proliferation AGAP2-AS1 inhibits CCA cell proliferation, colony formation, and promotes apoptosis. In addition, we also studied the molecular mechanism of AGAP2-AS1 in CCA cells and found potential targets.

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.

In addition, we demonstrated that AGAP2-AS1 promotes the proliferation of CCA. Conclusions: We conclude that the long non-coding RNA AGAP2-AS1 plays a role in promoting the proliferation of AGAP2-AS1 levels and clinicopathological features. Additionally, we investigated the functional impact of AGAP2-AS1 on tumor migration, invasion and proliferation during EOC progression through a series of in vitro and in vivo assays.

Overexpression of AGAP2-AS1 promoted cell growth, suppressed apoptosis, and caused trastuzumab resistance, whereas knockdown of AGAP2-AS1 showed an opposite effect. 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-AS1 in gastric cancer (GC) have not been characterized. AGAP2-AS1 was demonstrated as an oncogene in several cancers, including glioblastoma (GBM). 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.
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AGAP2-AS1 inhibits CCA cell proliferation, colony formation, and promotes apoptosis. In addition, we also studied the molecular mechanism of AGAP2-AS1 in CCA cells and found potential targets. Abstract Background Long noncoding RNAs (lncRNAs) have emerged as important regulators of tumorigenesis and cancer progression. 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.

4, ANRIL (CDKN2B antisense  9 Mar 2017 Additional file 1: Table S1. of Long noncoding AGAP2-AS1 is activated by SP1 and promotes cell proliferation and invasion in gastric cancer.
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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

miR-16-5p knockdown reversed the suppressive effects of AGAP2-AS1 knockdown in HCCLM3 cells (h-l). AGAP2-AS1 can increase NSCLC cell proliferation, migration and invasion, but inhibit NSCLC cell apoptosis. Mechanistically, AGAP2-AS1 can repress LATS2 and KLF2 transcription via binding with EZH2 and LSD1 .