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Hypermethylation-mediated silencing of NDRG4 promotes PDAC via regulating mitochondrial function
Hao-Hong Shi1 ( Research worker), Hai-E Liu1 ( Research worker), Xing-jing Luo 1,2,* (Professor)
1Department of Anesthesia, Children’s Hospital of Fudan University,
2Department of Anesthesia, Anhui Provincial Children’s Hospital
Abstract
The N-myc downstream regulated gene (NDRG) family members are dysregulated in multi tumor and functionally NDRGs play an important role in the malignant progression of cancer cells. However, little is known about the potential implications of NDRG4 in pancreatic ductal adenocarcinoma (PDAC). The aim of the current study was to elucidate the expression pattern of NDRG4 in PDAC and evaluate its potential cellular biological effects. Here, we firstly reported that epigenetic-mediated silencing of NDRG4 promotes PDAC via regulating mitochondrial function. Firstly, data mining demonstrated that NDRG4 was significantly down-regulated in PDAC tissue and cells, as well as, poor prognosis was existed in PDAC patients with low NDRG4 expression. What’s more, we uncovered that epigenetic regulation by DNA methylation was closely associated with NDRG4 down-regulation. NDRG4 overexpression dramatically suppressed PDAC cell growth and metastasis. Further functional analysis demonstrated that up-regulated NDRG4 in SW1990 and Canpan1 cells led to attenuated mitochondrial function, including reduced ATP production, decreased mitochondrial membrane potential and increased fragmented mitochondria. However, opposite results were received in HPNE cells treated NDRG4 knockdown. On the basis of the evidence above we deduce that hypermethylation-driven silencing of NDRG4 promotes PDAC via regulating mitochondrial function. And also NDRG4 could be as a potential biomarker for PDAC patients.
Abstract, Accepted Manuscript(in press) [Submitted on August 11, 2020, Accepted on November 17, 2020]
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