Erschienen in:
06.03.2020 | Original Article – Cancer Research
Relationship between DLEC1 and PBX3 promoter methylation and the risk and prognosis of gastric cancer in peripheral blood leukocytes
verfasst von:
Wenzhen Xie, Haibo Zhou, Qian Han, Tong Sun, Chuang Nie, Jia Hong, Rongrong Wei, Anastasiia Leonteva, Xu Han, Jing Wang, Xinyu Du, Lin Zhu, Yashuang Zhao, Wenjing Tian, Yingwei Xue
Erschienen in:
Journal of Cancer Research and Clinical Oncology
|
Ausgabe 5/2020
Einloggen, um Zugang zu erhalten
Abstract
Purpose
Aberrant DNA methylation could regulate the expression of tumor suppressor gene DLEC1 and oncogene PBX3 and was related to the occurrence and prognosis of gastric cancer (GC). In this study, the associations between DLEC1 and PBX3 promoter methylation in peripheral blood leukocytes (PBLs) and the risk and prognosis of GC were investigated.
Methods
The methylation status of DLEC1 and PBX3 promoter in PBLs of 368 GC cases and 382 controls was detected by the methylation-sensitive high-resolution melting (MS-HRM) method. Logistic and Cox regression were adopted to analyze the associations of DLEC1 and PBX3 methylation with GC risk and prognosis, respectively. Confounding biases were controlled by propensity score (PS).
Results
Compared with negative methylation (Nm), DLEC1-positive methylation (Pm) was associated with increased GC risk in PS (OR 2.083, 95% CI 1.220–3.558, P = 0.007), but PBX3 Pm was not associated with GC risk. In the elderly group (≥ 60 years), DLEC1 Pm was associated with increased GC risk (OR 2.951, 95% CI 1.426–6.104, P = 0.004). The combined effects between DLEC1 methylation and consumption of dairy products, fried food intake and Helicobacter pylori (H. pylori) infection on GC risk were discovered (ORc 3.461, 95% CI 1.847–6.486, P < 0.001, ORc 3.246, 95% CI 1.708–6.170, P < 0.001 and ORc 2.964, 95% CI 1.690–5.197, P < 0.001, respectively). Furthermore, DLEC1 and PBX3 methylation were not associated with GC prognosis.
Conclusion
DLEC1 methylation in PBLs and the combined effects of gene–environment can influence GC risk.