ArticleNaunyn-Schmiedeberg's archives of pharmacology2020
LncRNA HCP5 promotes LAML progression via PSMB8-mediated PI3K/AKT pathway activation.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- In Silico Drug Repurposing Against PSMB8 as a Potential Target for Acute Myeloid Leukemia Treatment.Molecular biotechnology · 2025Article
- The Proteasome-Family-Members-Based Prognostic Model Improves the Risk Classification for Adult Acute Myeloid Leukemia.Biomedicines · 2024Article
- LncRNA HCP5 Facilitates the Progression of Ovarian Cancer by Interacting with the PTBP1 Protein.Biochemical genetics · 2024Article
- Exosomal lncRNA HCP5 derived from human bone marrow mesenchymal stem cells improves chronic periodontitis by miR-24-3p/Heliyon · 2024Article
- Bioinformatics analysis identifiesAnnals of translational medicine · 2022Article
- N6-Methyladenosine-Related lncRNAs Are Novel Prognostic Markers and Predict the Immune Landscape in Acute Myeloid Leukemia.Frontiers in genetics · 2022Article
- Pan-cancer analysis of the prognostic and immunological role of PSMB8.Scientific reports · 2021Article
- HCP5, as the sponge of miR-1291, facilitates AML cell proliferation and restrains apoptosis via increasing PIK3R5 expression.Human genomics · 2021Article
- The adverse events of haematopoietic stem cell transplantation are associated with gene polymorphism within human leukocyte antigen region.Scientific reports · 2021Article
- Galectin-9 and PSMB8 overexpression predict unfavorable prognosis in patients with AML.Journal of Cancer · 2021Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia is an aggressive myeloid malignancy, characterized by rapid cellular proliferation and generally high mortality. Due to the lack of a complete understanding of AML, its clinical outcomes are still not satisfactory. In this study, we examined the function of the long non-coding RNA-HLA complex P5 (HCP5) on AML by analyzing the clinical samples, TCGA data, and by shRNA-mediated HCP5 deficiency in vitro. Our results showed that HCP5 is highly expressed in AML and is positive associated with poor prognosis, and HCP5 knockdown was significantly suppressing AML cell line proliferation and inducing G1/S arrest in vitro. In mechanism, the proteasome subunit beta type 8 (PSMB8) expression was dramatically inhibited in HCP5 knockdown cells while increased in HCP5 overexpression cells. PSMB8 was also highly expressed in AML and with poor prognosis. Furthermore, HCP5 regulates PI3K/AKT pathway activation depending on PSMB8. Our results showed a promoting function of HCP5 on AML and may provide a compelling biomarker and therapy target for AML.
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