High expression of DEK predicts poor prognosis of gastric adenocarcinoma

Piao, Jinhua; Shang, Yongjun; Liu, Shuangping; Piao, Yingshi; Cui, Xia; Li, Yuzi; Lin, Zhenhua

doi:10.1186/1746-1596-9-67

Cited by 37 publications

(33 citation statements)

References 27 publications

(35 reference statements)

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“…DEK mRNA expression has been reported in mouse (http://www.brain-map.org/) and human brains (Kroes et al 2000), but to our knowledge, no studies have investigated protein expression nor neuroanatomical distribution in distinct brain regions. In the human adult brain, DEK mRNA expression is more heavily expressed in malignant brain tumors relative to normal controls (Kroes et al 2000), consistent with the reported increase of DEK expression in various cancers including breast (Privette Vinnedge et al 2015), bladder (Datta et al 2011) and gastric (Piao et al 2014). DEK mRNA is also expressed throughout the brain in adolescent (PND56) male mice, which is consistent with our observations in adult mice.…”

Section: Discussionsupporting

confidence: 81%

“…Aberrant expression or localization of the DEK DNA-binding protein has been associated with several diseases, including acute myeloid leukemia (Logan et al 2015, Von Lindern et al 1992), various types of solid tumors (Piao et al 2014, Privette Vinnedge et al 2015, Wang et al 2014), and as an auto-antigen in numerous auto-immune diseases, most notably juvenile idiopathic arthritis (Mor-Vaknin et al 2011, Sierakowska et al 1993, Szer et al 1994). DEK (human 6p22.3) is a unique protein, with no known homologs, that preferentially binds supercoiled and cruciform DNA in vitro .…”

Section: Introductionmentioning

confidence: 99%

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Neuroanatomical Distribution of DEK Protein in Corticolimbic Circuits Associated with Learning and Memory in Adult Male and Female Mice

et al. 2018

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DEK, a chromatin-remodeling gene expressed in most human tissues, is known for its role in cancer biology and autoimmune diseases. DEK depletion in vitro reduces cellular proliferation, induces DNA damage subsequently leading to apoptosis, and down-regulates canonical Wnt/β-catenin signaling, a molecular pathway essential for learning and memory. Despite a recognized role in cancer (non-neuronal) cells, DEK expression and function is not well characterized in the central nervous system. We conducted a gene ontology analysis (ToppGene), using a cancer database to identify genes associated with DEK deficiency, which pinpointed several genes associated with cognitive-related diseases (i.e., Alzheimer’s disease, presenile dementia). Based on this information, we examined DEK expression in corticolimbic structures associated with learning and memory in adult male and female mice using immunohistochemistry. DEK was expressed throughout the brain in both sexes, including the medial prefrontal cortex (prelimbic, infralimbic and dorsal peduncular). DEK was also abundant in all amygdalar subdivisions (basolateral, central and medial) and in the hippocampus including the CA1, CA2, CA3, dentate gyrus (DG), ventral subiculum and entorhinal cortex. Of note, compared to males, females had significantly higher DEK immunoreactivity in the CA1, indicating a sex difference in this region. DEK was co-expressed with neuronal and microglial markers in the CA1 and DG, whereas only a small percentage of DEK cells were in apposition to astrocytes in these areas. Given the reported inverse cellular and molecular profiles (e.g., cell survival, Wnt pathway) between cancer and Alzheimer’s disease, these findings suggest a potentially important role of DEK in cognition.

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Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Neuroanatomical Distribution of DEK Protein in Corticolimbic Circuits Associated with Learning and Memory in Adult Male and Female Mice

et al. 2018

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“…11,12,16,17 Accordingly, DEK overexpression is significantly correlated with tumor growth, late pathological stage, and poor prognosis. [18][19][20][21] Although DEK has been studied in many tumor types, its expression and functions in astrocytic tumors are less known. In this study, we measured DEK expression in both normal brain tissues and astrocytic tumors.…”

Section: Introductionmentioning

confidence: 99%

DEK proto-oncogene is highly expressed in astrocytic tumors and regulates glioblastoma cell proliferation and apoptosis

Feng

Liu

et al. 2017

Tumour Biol.

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Astrocytic tumors are the most common neuroepithelial neoplasms with high relapse rate after surgery. Understanding the molecular mechanisms for astrocytic tumorigenesis and progression will lead to early diagnosis and effective treatment of astrocytic tumors. The DEK mRNA and protein expression in normal brain tissues and astrocytic tumors was quantified. To investigate DEK functions in tumor cells, DEK gene was silenced with siRNA in U251 glioblastoma cells. Cell proliferation, cell cycle and apoptosis were then measured. The expression and activity of key genes that regulate cell proliferation and apoptosis were also measured. We identified DEK as a high expressed gene in astrocytic tumor tissues. DEK expression level was positively correlated with the pathological grade of astrocytic tumors. Gene silencing of DEK in U251 glioblastomas inhibited cell proliferation and blocked cells at G0/G1 phase of cell cycle. DEK depletion also induced cell apoptosis, with up-regulated expression of P53 and P21 and down-regulated expression of Bcl-2 and C-myc. The Caspase-3 activity in U251 cells was also significantly increased after knockdown. Our results provided evidences that DEK regulates proliferation and apoptosis of glioblastomas. DEK gene silencing may induce apoptosis through P53-dependent pathway. Our data indicated DEK plays multiple roles to facilitate tumor growth and maintenance. It can be used as a potential target for astrocytic tumor diagnosis and gene therapy.

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“…DEK can promote the repair of DNA damage while also participates in apoptosis [6]. DEK has been already identified as an oncogene and is overexpressed in various malignant tumors, such as colorectal, gastric, neuroendocrine, prostate, breast, and bladder cancer [7][8][9][10][11]. Recent studies indicate that DEK depletion induced astrocytic tumor cell apoptosis with down-regulated expression of Bcl-2 and C-myc; the caspase-3 activity in the astrocytic tumor was also significantly enhanced after the knockdown [12].…”

Section: Introductionmentioning

confidence: 99%

The miR-1204 regulates apoptosis in NSCLC cells by targeting DEK

Qian

Yang

Liu

et al. 2019

Folia Histochem Cytobiol.

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Introduction. This study endeavors to analyze the effects of miR-1204 on the expression of DEK oncogene in non-small cell lung cancer (NSCLC) cell lines and to study the molecular mechanisms of these effects. Material and methods. The miR-1204 mimics and inhibitors were transfected into the (A549 and SPC) NSCLC cells. Then the mRNA levels, cell viability, apoptosis rate, morphology and caspase activity were determined. The expression of apoptosis-related proteins Bcl-2 and Bax was also analyzed. Results. In NSCLC cell lines (A549 and SPC), DEK mRNA levels were down-regulated in miR-1204 overexpression group. In miR-1204 inhibition group, the expression of DEK mRNA showed an opposite trend. The overexpression of miR-1204 increases the apoptosis rate in NSCLC cells. The Bcl-2 level in the miR-1204 overexpression group was decreased, while the Bax level was increased. In the miR-1204 inhibition group, expression of Bcl-2 and Bax showed opposite trends. Cell staining revealed cell's morphological changes; the apoptosis in the miR-1204 overexpression group revealed significant morphological features, such as brighter nuclei and nuclear condensation. Results indicated a typical characteristic of apoptosis in the miR-1204 overexpression group. Caspase-9 and Caspase-3 were involved in the apoptosis pathway, which was mediated by miR-1204 and DEK. Conclusions. The miR-1204 induces apoptosis of NSCLC cells by inhibiting the expression of DEK. The mechanism of apoptosis involves down-regulation of Bcl-2 and up-regulation of Bax expression. Moreover, the apoptosis was mediated by mitochondria-related caspase 9/3 pathway.

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High expression of DEK predicts poor prognosis of gastric adenocarcinoma

Cited by 37 publications

References 27 publications

Neuroanatomical Distribution of DEK Protein in Corticolimbic Circuits Associated with Learning and Memory in Adult Male and Female Mice

Neuroanatomical Distribution of DEK Protein in Corticolimbic Circuits Associated with Learning and Memory in Adult Male and Female Mice

DEK proto-oncogene is highly expressed in astrocytic tumors and regulates glioblastoma cell proliferation and apoptosis

The miR-1204 regulates apoptosis in NSCLC cells by targeting DEK

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