High expression of CPNE3 predicts adverse prognosis in acute myeloid leukemia

Abstract

CPNE3, a member of a Ca2+‐dependent phospholipid‐binding protein family, was identified as a ligand of ERBB2 and has a more general role in carcinogenesis. Here, we identified the prognostic significance of CPNE3 expression in acute myeloid leukemia (AML) patients based on two datasets. In the first microarray dataset (n = 272), compared to low CPNE3 expression (CPNE3 low), high CPNE3 expression (CPNE3 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), CPNE3 high was also associated with adverse OS and EFS (OS, P = 0.01; EFS, P = 0.036). Notably, among CPNE3 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 CPNE3 low patients (allogeneic HCT, n = 32 vs chemotherapy, n = 54). These results indicated that CPNE3 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/microRNA expression signatures and cell signaling pathways associated with CPNE3 expression. In conclusion, CPNE3 high is an adverse prognostic biomarker for AML. Its effect may be attributed to the distinctive genome‐wide gene/microRNA expression and related cell signaling pathways.

Silencing the expression of copine-III enhances the sensitivity of hepatocellular carcinoma cells to the molecular targeted agent sorafenib

“…Lin et al found the metastasis-promoting roles of copine-III in non-small cell lung cancer (NSCLC) via a quantitative proteomic analysis 26. Recently, Fu et al reported that high expression of CPNE3 predicts adverse prognosis in AML 27. Our results showed that copine-III would participate in sorafenib-resistance in advanced HCC treatment.…”

“… 26 Recently, Fu et al reported that high expression of CPNE3 predicts adverse prognosis in AML. 27 Our results showed that copine-III would participate in sorafenib-resistance in advanced HCC treatment. These data expand our understanding of copine-III in human cancers.…”

CPNE3 promotes migration and invasion in non-small cell lung cancer by interacting with RACK1 via FAK signaling activation

“…Moreover, CPNE3 plays a pivotal role in other diseases. High expression of CPNE3 predicted an adverse prognosis in acute myeloid leukemia 12 , and it was identified as a novel candidate gene for schizophrenia 13 . However, in NSCLC, the underlying mechanism of CPNE3 remains unknown.…”

Proteomic Studies of Primary Acute Myeloid Leukemia Cells Derived from Patients Before and during Disease-Stabilizing Treatment Based on All-Trans Retinoic Acid and Valproic Acid

“…Overlap of differentially regulated phosphorylation sites from the current PRE-R vs. PRE-NR study with those identified in previously published MS-based phosphoproteomics studies; Table S1: Proteomic differences between AML patients when comparing AML cells derived from responders vs. non-responders to antileukemic treatment based on ATRA and VP; Table S2: Regulated proteins that have both phosphorylation and expression fold change (FC) in the PRE-R vs. PRE-NR study; Table S3: Pair-wised fold change (FC) of regulated protein expression in responder patients considering quantitative values at pre-treatment (PRE), day 3 (3D) and day 8 (8D) of the ATRA–VP–TP treatment; Table S4: Pair-wised fold change (FC) of regulated protein expression in non-responder patients considering quantitative values at pre-treatment (PRE), day 3 (3D) and day 8 (8D) of the ATRA–VP–TP treatment; Table S5: Pair-wised fold change (FC) of differentially regulated phosphorylation sites in responder patients considering quantitative values at pre-treatment (PRE), day 3 (3D) and day 8 (8D) of the ATRA–VP–TP treatment; Table S6: Pair-wised fold change of differentially regulated phosphorylation sites in non-responder patients considering quantitative values at pre-treatment (PRE), day 3 (3D) and day 8 (8D) of the ATRA–VP–TP treatment. References [ 26 , 48 , 49 , 53 , 71 , 90 , 113 , 114 , 115 , 116 , 117 , 118 , 119 , 120 , 121 , 122 , 123 , 124 , 125 , 126 , 127 , 128 , 129 , 130 , 131 , 132 , 133 , 134 , 135 , 136 , 137 , 138 , 139 , 140 , 141 , 142 , 143 …”