Synergistic Role between p53 and JWA: Prognostic and Predictive Biomarkers in Gastric Cancer

Liu, Xin; Wang, Shouyu; Xia, Xiaowei; Chen, Yansu; Zhou, Yan; Wu, Xuming; Zhang, Jianbing; He, Song; Tan, Yongfei; Fu, Qiang; Røe, Oluf Dimitri; Li, Gang; Zhou, Jianwei

doi:10.1371/journal.pone.0052348

Cited by 20 publications

(18 citation statements)

References 47 publications

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“…Furthermore, our present data revealed that PDCD2 expression was associated with prolonged survival of patients with gastric cancer, whereas p53 expression was associated with poor prognosis of gastric cancer. The latter data were consistent with those of previous literature reports (18,19). The former data are novel and have not been reported by any study in the present PubMed database.…”

Section: Discussionsupporting

confidence: 94%

Programmed cell death 2 protein induces gastric cancer cell growth arrest at the early S phase of the cell cycle and apoptosis in a p53-dependent manner

et al. 2014

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Abstract. Programmed cell death 2 (PDCD2) is a highly conserved nuclear protein, and aberrant PDCD2 expression alters cell apoptosis. The present study aimed to investigate PDCD2 expression in gastric cancer. Tissue specimens from 34 gastric cancer patients were collected for analysis of PDCD2 expression using immunohistochemistry, western blotting and qRT-PCR. Gastric cancer cell lines (a p53-mutated MKN28 line and a wild-type p53 MKN45 line) were used to assess the effects of PDCD2 overexpression. p53 -/-nude mice were used to investigate the effect of PDCD2 on ultraviolet B (UVB)-induced skin carcinogenesis. The data showed that PDCD2 expression was reduced in gastric cancer tissue specimens, and loss of PDCD2 expression was associated with the poor survival of patients. PDCD2 expression induced gastric cancer cell growth arrest at the early S phase of the cell cycle and apoptosis. The antitumor effects of PDCD2 expression were dependent on p53 expression in gastric cancer cells. Moreover, PDCD2 expression inhibited activity of the ATM/Chk1/2/p53 signaling pathway. In addition, PDCD2 expression suppressed UVB-induced skin carcinogenesis in p53 +/+ nude mice, but not in p53 -/-mice. The data from the present study demonstrated that loss of PDCD2 expression could contribute to gastric cancer development and progression and that PDCD2-induced gastric cancer cell growth arrest at the early S phase of the cell cycle and apoptosis are p53-dependent.

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Section: Discussionsupporting

confidence: 94%

Programmed cell death 2 protein induces gastric cancer cell growth arrest at the early S phase of the cell cycle and apoptosis in a p53-dependent manner

et al. 2014

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“…Similar to the present study, Chung et al (24) reported that there was no specific genotype of P53 polymorphism in a gastric cancer cohort compared with other groups with or without H. pylori-associated chronic gastritis in a Korean population, though another study by Liu et al identified a significant difference between P53 expression in primary tumor and non-tumor tissue in gastric cancer patients (25). In the gastric cancer group in the current study, the male to female ratio was 1.56, and there was no significant difference in sex distribution between the case and control groups.…”

Section: Discussionsupporting

confidence: 86%

Association of P53 gene polymorphism with gastric cancer in Northern Iran as a high‑risk region

et al. 2018

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Abstract. Gastric cancer has the fourth highest morbidity rate of all cancers worldwide. Genetic factors including alterations in oncogenes and tumor suppressor genes serve an important role in gastric cancer development and progression. The P53 gene acts as a tumor suppressor gene by regulating the cell cycle, DNA transcription and repair, apoptosis, senescence and genome stability. In addition to somatic P53 mutations in cancer development, germline polymorphisms are also involved in different malignancies. The polymorphism of P53 at codon 72 (Arg72Pro) is established as a common variant that increases susceptibility to various cancers. The present case-control study was conducted to evaluate the possible association between this P53 polymorphism and gastric cancer in the Iranian population. A total of 59 patients with gastric cancer and 59 healthy controls were enrolled in the present study. Genomic DNA was extracted from peripheral blood mononuclear cells and genotype analysis was performed using a polymerase chain reaction-based restriction fragment length polymorphism assay. Genotype frequencies did not differ significantly between the patients and controls (P=0.4); the frequencies of the three genotypes Arg/Arg, Arg/Pro and Pro/Pro in gastric cancer patients were 28.8, 49.2 and 22.0%, and in controls were 37.3, 49.2 and 13.6%. Additionally, there were no differences in genotype frequencies based on tumor location, histological differentiation or tumor stage. Based on these findings, it may be concluded that the P53 codon 72 polymorphism does not contribute to gastric cancer susceptibility in Northern Iran. IntroductionGastric cancer has the third highest mortality and fourth highest morbidity rates of all cancers worldwide (1). In 2012, GloboCan statistics reported almost 1 million new cases of gastric cancer, and more than 700,000 mortalities caused by gastric cancer (1). Gastric cancer is a multifactorial disorder, in which genetic and environmental interactions serve an important role in development and progression (2). Increasing age, gender, lifestyle, dietary regime, environmental factors and Helicobacter pylori infections are among the known risk factors for stomach cancer (3,4). While dietary regime and lifestyle are the most recognized factors, more effective identification of the genetic risk factors is expected to improve understanding of the basic molecular events involved in tumorigenesis (5). Various genetic and epigenetic changes that have the potential to convert normal epithelial cells in the stomach into malignant neoplasms may be responsible for the development of both familial and sporadic gastric cancer (6,7). Studies performed recently have demonstrated that a high number of genes and various environmental factors are the causal agents of gastric cancer, and the presence of different forms of alleles in genes (polymorphisms) may promote the development of cancers; in this regard, the P53 gene has been a research focus due to its role as a major tumor suppressor gene (8,9). The P53 ge...

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“…Overexpression of mutated p53 has been correlated with pathological parameters of tumour aggressiveness and poor prognosis in human gastric carcinoma [9]. …”

Section: Introductionmentioning

confidence: 99%

An immunohistochemical study of canine spontaneous gastric polyps

et al. 2014

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BackgroundGastric polyps (GP) are characterised by luminal overgrowths projecting above the plane of the mucosal surface that can be classified as non-neoplastic and neoplastic lesions. In humans, recent studies have drawn attention to the malignant potential of some of these lesions. However, gastric polyps are uncommon lesions in dogs.FindingsIn this study, the presence of Helicobacter spp., the cellular proliferative activity, potential phenotypic alterations, COX-2 and p53 expression in canine spontaneous gastric polyps were investigated. The expression of these molecules was also studied in normal canine gastric mucosa in order to gain further knowledge of the significance of their loss or overexpression in gastric lesions.ConclusionsThe normal expression of almost all the factors evaluated, along with the reduced proliferative activity is strongly suggestive that, in dogs, spontaneous gastric polyps are not only a rare finding but also of benign nature.Virtual SlidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/13000_2014_166

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Synergistic Role between p53 and JWA: Prognostic and Predictive Biomarkers in Gastric Cancer

Cited by 20 publications

References 47 publications

Programmed cell death 2 protein induces gastric cancer cell growth arrest at the early S phase of the cell cycle and apoptosis in a p53-dependent manner

Programmed cell death 2 protein induces gastric cancer cell growth arrest at the early S phase of the cell cycle and apoptosis in a p53-dependent manner

Association of P53 gene polymorphism with gastric cancer in Northern Iran as a high‑risk region

An immunohistochemical study of canine spontaneous gastric polyps

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