tr A2BDH2 A2BDH2_PONAB Major prion protein OS=Pongo

Gene ID Unique ID sequence Library number Human

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.

Agap2-as1

2018 ). AGAP2-AS1 promoted cell growth, suppressed apoptosis, and caused trastuzumab resistance, whereas knockdown of AGAP2-AS1 showed an opposite effect. MyD88 was identified as a downstream target of AGAP2-AS1 and mediated the AGAP2-AS1-induced oncogenic effects. Mechanistically, the RIP assay revealed that AGAP2-AS1 could bind to CBP, a As the antisense lncRNA of AGAP2, AGAP2-AS1 was found to conversely inhibited cell proliferation and metastasis in EOC cell lines, and low expression of AGAP2-AS1 was correlated with tumor malignant features, indicating that AGAP2-AS1 is a potential tumor suppressor of EOC. Interestingly, AGAP2‐AS1 sponges miR‐4,668‐3p to release SRSF1 in CRC. Furthermore, in the rescue functional assay, miR‐4,668‐3p down‐regulation exacerbated the malignant behaviors of AGAP2‐AS1‐depleted CRC cells, whereas such effects were further offset by SRSF1 knockdown.

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).

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Your search resulted in multiple matches. Please select a position: Gencode Genes AGAP2-AS1 (ENST00000542466.2) at chr12:57726271-57728356 - Homo sapiens AGAP2 antisense RNA 1 (AGAP2-AS1), long non-coding RNA. 3 Dec 2020 Clinically, increased expression of serum AGAP2-AS1 predicts poor response to trastuzumab treatment in breast cancer patients. In conclusion, 2 Mar 2021 LncRNA AGAP2-AS1 Promotes Cancer Cell Proliferation, Migration and Invasion in Colon Cancer by Forming a Negative Feedback Loop with 2 Mar 2021 LncRNA AGAP2-AS1 Promotes Cancer Cell Proliferation, Migration and Invasion in Colon Cancer by Forming a Negative Feedback Loop with HGNC data for AGAP2-AS1.

Human_LncRNA_Seq1 A B C D E F G H I J K L 1 Type 2

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. 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 Prostate cancer remains a significant cause of cancer-related deaths in male population.

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. Moreover, we also explored the molecular events that occurred AGAP2-AS1 was up-regulated and associated with poor prognosis in GBM. Knockdown of AGAP2 -AS1 suppressed proliferation and invasion, and facilitated apoptosis in GBM cells . To explore the functional relevance of AGAP2AS1 in - GBM cells, we interfered endogenous AGAP2-AS1 expression in U87/MG and U251/MG cells by 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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High AGAP2-AS1 expression may predict a poor prognosis in GBM patients.

GeneCards - The Human Gene Compendium 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. Results: 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 … AGAP2-AS1 was upregulated in MSC-cultured cells, and knockdown of AGAP2-AS1 reversed the MSC-mediated trastuzumab resistance.
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tr A2BDH2 A2BDH2_PONAB Major prion protein OS=Pongo

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Journal of Cell Science. 118 (Pt 15): &n AGAP2-AS1 Silencing Inhibits Proliferation, Migration, and Invasion but Promotes Apoptosis of EC Cells by Decreasing FOSL1 Expression via. Upregulation of 12, ENSG00000229950, TFAP2A-AS1, 1.70E-15, 8.59E-13, 1.89. 13, ENSG00000138792 246, ENSG00000255737, AGAP2-AS1, 8.44E-10, 1.70E-07, -1.53. AFAP1L1, AFAP1L2, AFDN, AFF1, AFF2, AFF3, AFF4, AFG3L2, AFMID, AFTPH, AGA, AGAP1, AGAP2, AGAP2-AS1, AGAP3, AGBL5, AGFG1, AGFG2, AGGF1 AGAP2-AS1 100130776 AGAP2 antisense RNA 112.

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The trend of expression was confirmed with RT-PCR.The correlation between sample status as either progressor or non-progressor and AGAP2-AS1 level was R 2 =0.69, p<0.01. 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).

CCK-8 assay was used to detect cell proliferation. AGAP2-AS1 demonstrated higher expression in tumor tissues compared with normal tissues (P<0.001; Fig. 1A).