Differential expression of calcium-related genes in gastric cancer cells transfected with cellular prion protein

Liang, Jie; Luo, Guanhong; Ning, Xiaoxuan; Shi, Yongquan; Zhai, Huihong; Sun, Shan; Jin, Haifeng; Liu, Zhenxiong LiuZ.; Zhang, Faming ZhangF.; Lu, Yuanyuan; Zhao, Yunping; Chen, Xiong ChenX.; Zhang, Hongbo ZhangH.; Guo, Xi; Wu, Kaichun; Fan, Daiming

doi:10.1139/o07-052

Cited by 25 publications

(24 citation statements)

References 30 publications

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“…Fewer studies have used a similar approach to try to understand the biological function of the PrP protein in immortalized non-neuronal cells [25-27]. The obtained results appear again to correlate with the cell line used as experimental model and no shared pathway has emerged from the comparison of these different experiments.…”

Section: Introductionmentioning

confidence: 92%

Brain transcriptional stability upon prion protein-encoding gene invalidation in zygotic or adult mouse

et al. 2010

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BackgroundThe physiological function of the prion protein remains largely elusive while its key role in prion infection has been expansively documented. To potentially assess this conundrum, we performed a comparative transcriptomic analysis of the brain of wild-type mice with that of transgenic mice invalidated at this locus either at the zygotic or at the adult stages.ResultsOnly subtle transcriptomic differences resulting from the Prnp knockout could be evidenced, beside Prnp itself, in the analyzed adult brains following microarray analysis of 24 109 mouse genes and QPCR assessment of some of the putatively marginally modulated loci. When performed at the adult stage, neuronal Prnp disruption appeared to sequentially induce a response to an oxidative stress and a remodeling of the nervous system. However, these events involved only a limited number of genes, expression levels of which were only slightly modified and not always confirmed by RT-qPCR. If not, the qPCR obtained data suggested even less pronounced differences.ConclusionsThese results suggest that the physiological function of PrP is redundant at the adult stage or important for only a small subset of the brain cell population under classical breeding conditions. Following its early reported embryonic developmental regulation, this lack of response could also imply that PrP has a more detrimental role during mouse embryogenesis and that potential transient compensatory mechanisms have to be searched for at the time this locus becomes transcriptionally activated.

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Section: Introductionmentioning

confidence: 92%

Brain transcriptional stability upon prion protein-encoding gene invalidation in zygotic or adult mouse

et al. 2010

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“…Interestingly, S100P mRNA can be measured in saliva, and aids in the diagnosis of oral cancer (Li et al 2004). S100P is also expressed in gastric cancer (Shyu et al 2003; Liang et al 2007) and appears to function to increase the growth and invasion of the cancer cells (Namba et al 2009). …”

Section: S100p In Different Cancersmentioning

confidence: 99%

S100P: a novel therapeutic target for cancer

2010

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S100P expression is described in many different cancers, and its expression is associated with drug resistance, metastasis, and poor clinical outcome. S100P is member of the S100 family of small calcium-binding proteins that have been reported to have either intracellular or extracellular functions, or both. Extracellular S100P can bind with the receptor for advanced glycation end products (RAGE) and activate cellular signaling. Through RAGE, S100P has been shown to mediate tumor growth, drug resistance, and metastasis. S100P is specifically expressed in cancer cells in the adult. Therefore, S100P is a useful marker for differentiating cancer cells from normal cells, and can aid in the diagnosis of cancer by cytological examination. The expression of S100P in cancer cells has been related to hypomethylation of the gene. Multiple studies have confirmed the beneficial effects of blocking S100P/RAGE in cancer cells, and different blockers are being developed including small molecules and antagonist peptides. This review summarizes the role and significance of S100P in different cancers.

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“…Starting from these observations PrP C has been intriguingly involved in the development of human tumors [22, 31], including glioblastoma [32, 33], and gastric [34], breast [35], prostate [36], and colorectal [37] carcinomas. For example, PrP C expression was correlated with increased cell proliferation in gastric cancer cell lines [18, 38], and PrP C overexpression was shown to provide cancer cells with resistance to cytotoxic agents [36], and higher invasive properties [39]. …”

Section: Introductionmentioning

confidence: 99%

Cellular prion protein controls stem cell-like properties of human glioblastoma tumor-initiating cells

et al. 2016

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Prion protein (PrPC) is a cell surface glycoprotein whose misfolding is responsible for prion diseases. Although its physiological role is not completely defined, several lines of evidence propose that PrPC is involved in self-renewal, pluripotency gene expression, proliferation and differentiation of neural stem cells. Moreover, PrPC regulates different biological functions in human tumors, including glioblastoma (GBM). We analyzed the role of PrPC in GBM cell pathogenicity focusing on tumor-initiating cells (TICs, or cancer stem cells, CSCs), the subpopulation responsible for development, progression and recurrence of most malignancies. Analyzing four GBM CSC-enriched cultures, we show that PrPC expression is directly correlated with the proliferation rate of the cells. To better define its role in CSC biology, we knocked-down PrPC expression in two of these GBM-derived CSC cultures by specific lentiviral-delivered shRNAs. We provide evidence that CSC proliferation rate, spherogenesis and in vivo tumorigenicity are significantly inhibited in PrPC down-regulated cells. Moreover, PrPC down-regulation caused loss of expression of the stemness and self-renewal markers (NANOG, Sox2) and the activation of differentiation pathways (i.e. increased GFAP expression). Our results suggest that PrPC controls the stemness properties of human GBM CSCs and that its down-regulation induces the acquisition of a more differentiated and less oncogenic phenotype.

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Differential expression of calcium-related genes in gastric cancer cells transfected with cellular prion protein

Cited by 25 publications

References 30 publications

Brain transcriptional stability upon prion protein-encoding gene invalidation in zygotic or adult mouse

Brain transcriptional stability upon prion protein-encoding gene invalidation in zygotic or adult mouse

S100P: a novel therapeutic target for cancer

Cellular prion protein controls stem cell-like properties of human glioblastoma tumor-initiating cells

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