1. Academic Validation
  2. Long noncoding RNA LINC00265 predicts the prognosis of acute myeloid leukemia patients and functions as a promoter by activating PI3K-AKT pathway

Long noncoding RNA LINC00265 predicts the prognosis of acute myeloid leukemia patients and functions as a promoter by activating PI3K-AKT pathway

  • Eur Rev Med Pharmacol Sci. 2018 Nov;22(22):7867-7876. doi: 10.26355/eurrev_201811_16412.
L Ma 1 W-X Kuai X-Z Sun X-C Lu Y-F Yuan
Affiliations

Affiliation

  • 1 Department of Pediatrics, The Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu, China. mma33166@163.com.
Abstract

Objective: Mounting evidence suggests that long noncoding RNAs (lncRNAs) function in multiple cancers. This study aimed to determine the expression, clinical significance, and possible biological function of a novel lncRNA LINC00265 in acute myeloid leukemia (AML).

Patients and methods: The expression levels of LINC00265 were systematically evaluated in TCGA datasets. RT-PCR was performed to examine the expression level of LINC00265 in bone marrow and serum obtained from AML patients and healthy controls. The clinical data were interpreted by x2 test, Kaplan-Meier analyses, univariate analysis, and multivariate analysis. The functional role of LINC00265 was verified using cell experiments. Western blotting was used to examine the modulatory effect of LINC00265 on Akt/PI3K pathway in AML.

Results: LINC00265 was significantly highly expressed in the bone marrow and serum of AML patients. High serum LINC00265 was significantly associated with FAB classification and cytogenetics. ROC analyses showed that serum LINC00265 levels were reliable in distinguishing patients with AML from normal controls. Clinical assay indicated that AML patients with higher serum LINC00265 expression suffered poorer overall survival. Functionally, overexpression of LINC00265 suppressed the capability of proliferation, migration and invasion in AML cell lines. By using Western blot, we further illustrated that LINC00265 activated PI3K/Akt signaling in AML cell lines.

Conclusions: Our findings not only demonstrated that LINC00265 contributes to AML proliferation, migration and invasion via modulation of PI3K/Akt signaling, but also suggested the potential value of LINC00265 as a clinical prognostic and a diagnostic marker for AML.

Figures
Products