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.
