Open AccessHigh expression of CPNE 3 predicts adverse prognosis in acute myeloid leukemia
Author(s) -
Fu Lin,
Fu Huaping,
Qiao Jianlin,
Pang Yifan,
Xu Keman,
Zhou Lei,
Wu Qingyun,
Li Zhenyu,
Ke Xiaoyan,
Xu Kailin,
Shi Jinlong
Publication year - 2017
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.13311
Subject(s) - myeloid leukemia , adverse effect , oncology , medicine , carcinogenesis , myeloid , chemotherapy , microarray , cancer research , gene expression , biology , gene , cancer , genetics
CPNE 3 , a member of a Ca 2+ ‐dependent phospholipid‐binding protein family, was identified as a ligand of ERBB 2 and has a more general role in carcinogenesis. Here, we identified the prognostic significance of CPNE 3 expression in acute myeloid leukemia ( AML ) patients based on two datasets. In the first microarray dataset ( n = 272), compared to low CPNE 3 expression ( CPNE 3 low ), high CPNE 3 expression ( CPNE 3 high ) was associated with adverse overall survival ( OS , P < 0.001) and event‐free survival ( EFS , P < 0.001). In the second independent group of AML patients ( TCGA dataset, n = 179), CPNE 3 high was also associated with adverse OS and EFS ( OS , P = 0.01; EFS , P = 0.036). Notably, among CPNE 3 high patients, those received allogenic hematopoietic cell transplantation ( HCT ) had longer OS and EFS than those with chemotherapy alone (allogeneic HCT , n = 40 vs chemotherapy, n = 46), but treatment modules played an insignificant role in the survival of CPNE 3 low patients (allogeneic HCT , n = 32 vs chemotherapy, n = 54). These results indicated that CPNE 3 high is an independent, adverse prognostic factor in AML and might guide treatment decisions towards allogeneic HCT . To understand its inherent mechanisms, we investigated genome‐wide gene/micro RNA expression signatures and cell signaling pathways associated with CPNE 3 expression. In conclusion, CPNE 3 high is an adverse prognostic biomarker for AML . Its effect may be attributed to the distinctive genome‐wide gene/micro RNA expression and related cell signaling pathways.