PLCB4 upregulation is associated with unfavorable prognosis in pediatric acute myeloid leukemia.

Abstract:

:Phospholipase C (PLC) is a membrane-associated enzyme that regulates several cellular behaviors including cell motility, growth, transformation and differentiation. PLC is involved in cancer migration, invasion and drug resistance. However, the expression status and prognostic role of PLCB4 in acute myeloid leukemia (AML) remain unclear. In the present study, the complete clinical and mRNA expression data of 285 pediatric patients with de novo AML were obtained from the Therapeutically Available Research to Generate Effective Treatments database. The association between PLCB4 expression and clinical and molecular features was explored. The expression of PLCB4 was significantly higher in patients with AML who relapsed compared with those with long-term complete remission. Patients with PLCB4 upregulation had significantly lower overall survival (OS) and event free survival (EFS) rate compared with those with low PLCB4 expression. Multivariate Cox's regression analyses demonstrated that high PLCB4 expression was an independent risk factor of adverse OS (P<0.01; HR, 2.081) and EFS (P<0.01; HR, 2.130). Following stratification analysis according to transplant status in cases of first complete remission, the patients with high expression of PLCB4 had significantly lower OS and EFS rate in the chemotherapy group, but not the stem cell transplant group. Furthermore, PLCB4-associated genes were identified using Spearman's rank correlation analysis. KEGG pathway analysis revealed that PLCB4 and its associated genes were mainly involved in three potential pathways, including the Rap1 signaling pathway. Overall, the findings of the present study suggest that increased PLCB4 expression is associated with poor clinical outcome in pediatric patients with AML, and thus may represent a potential prognostic biomarker and therapeutic target for AML.

journal_name

Oncol Lett

journal_title

Oncology letters

authors

Wu S,Zhang W,Shen D,Lu J,Zhao L

doi

10.3892/ol.2019.10921

subject

Has Abstract

pub_date

2019-12-01 00:00:00

pages

6057-6065

issue

6

eissn

1792-1074

issn

1792-1082

pii

OL-0-0-10921

journal_volume

18

pub_type

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