ArticleAmerican journal of translational research2023
AGAP2-AS1/BRD7/c-Myc signaling axis promotes skin cutaneous melanoma progression.
Article in American journal of translational research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- The role of non-coding RNAs in the regulation of cell death pathways in melanoma.Discover oncology · 2025Review
- Brachyury promotes proliferation and migration of colorectal cancer cells by targeting MMP14.Cancer cell international · 2025Article
- MTMR7 regulates human spermatogonial stem cells proliferation and migration via targeting FLNB.PloS one · 2025Article
- LINC01320 facilitates cell proliferation and migration of ovarian cancer via regulating PURB/DDB2/NEDD4L/TGF-β axis.Scientific reports · 2024Article
- Long Non-Coding RNAMolecules (Basel, Switzerland) · 2024Review
- Long non-coding RNA VCAN-AS1 promotes gastric cancer progression via the HuR/F11R pathway.American journal of translational research · 2024Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo examine the effects and mechanisms of AGAP2 Antisense RNA 1 (AGAP2-AS1) in progression of skin cutaneous melanoma (SKCM).
methodsAGAP2-AS1 expression and SKCM survival outcomes were assessed using bioinformatics analysis. In vitro and in vivo assays, including cell proliferation, colony formation, migration, and tumor formation assays, were performed to detect AGAP2-AS1 oncogenic effects in SKCM. RNA pull-down, RNA immunoprecipitation (RIP), and co-immunoprecipitation were used to evaluate the mechanism of AGAP2-AS1 in SKCM progression.
resultsAGAP2-AS1 was upregulated in human SKCM tissues and cells and predicted a worse prognosis. AGAP2-AS1 silencing in two SKCM cell lines inhibited cell proliferation, as well as colony formation and migration both in vitro and in vivo. The RNA pull-down assay and RIP analysis results indicated that AGAP2-AS1 interacted with bromodomain containing 7 (BRD7). AGAP2-AS1 knockdown attenuated the BRD7 and c-Myc interaction, which reduced c-Myc expression. The altered phenotypes found in AGAP2-AS1- and BRD7-deficient cells were rescued by overexpression of c-Myc.
conclusionsAGAP2-AS1 participated in oncogenesis in SKCM via the BRD7/c-Myc signaling pathway. These results suggest a molecular mechanism for AGAP2-AS1 in the carcinogenesis of SKCM.
Indexed as
Identifiers
36777828PMC9908487What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.