Expression of the periostin mRNA level in neuroblastoma☆
Section snippets
Patients
The study groups included 24 (14 boys, 10 girls) neuroblastoma patients who had undergone surgery at the Department of Surgery II, Nagoya City University Medical School between 1989 and 2000. The neuroblastomas were classified according to the International Neuroblastoma Staging System. Of the 24 cases, 18 were identified at less than 1 year of age, and 18 of the 24 infantile patients were identified by a mass screening system (Table 1).All tumor samples were collected at resection and
Periostin mRNA expression
Of 24 neuroblastomas studied, all of the tumor samples had periostin transcript, and the periostin/GAPDH mrRNA level was 33.231 ± 48.140 (mean ± SD). The relationship between the gene expression of periostin in neuroblastoma and the patients' clinicopathologic factors is shown in Table 1. There was no significant difference in the periostin expression between patient groups stratified according to the gender. The periostin mRNA level was significantly higher in the group diagnosed by symptom
Discussion
In the current study, periostin mRNA expression was analyzed for the first time in clinical samples of neuroblastoma. We have shown that periostin mRNA level was higher in the groups identified by symptoms or after 1 year of age in neuroblastoma. It has been shown previously that the human periostin gene is overexpressed in the lung carcinomas and correlated with worse prognosis. We showed that mRNA expression of periostin was relatively higher in the tumor with the advanced stage of
Acknowledgements
The authors thank Mrs A. Miyazaki for her excellent technical assistance.
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2022, Cell ReportsCitation Excerpt :Pearson’s correlation coefficient analyses revealed significant positive correlations of expression between EP2 and a large proportion of these cytokines, chemokines, growth factors, and receptors (40/45, ∼89%) in at least two of the four major R2 NB datasets: SEQC, Kocak, Versteeg, and NRC (Figure 1D). These potential NB facilitators include ALK (Trigg and Turner, 2018), brain-derived neurotrophic factor (BDNF) (Middlemas et al., 1999), chemokine (C-C motif) ligand 2 (CCL2) or monocyte chemoattractant protein 1 (MCP-1)/C-C chemokine receptor type 2 (CCR2) (Metelitsa et al., 2004), colony-stimulating factor 1 (CSF-1)/CSF-1 receptor (CSF1R) (Webb et al., 2018), chemokine (C-X3-C motif) ligand 1 (CX3CL1)/CX3CR1 (Nevo et al., 2009), CXCL2/CXCR2 (Hashimoto et al., 2016), CXCL12/CXCR4/CXCR7 (Liberman et al., 2012), epidermal growth factor receptor (EGFR) (Ho et al., 2005), endoglin (ENG) or cluster of differentiation 105 (CD105) (Cavar et al., 2015; Pezzolo et al., 2007; Wu et al., 2019), glial cell line-derived neurotrophic factor (GDNF)/GDNF family receptor α1 (GFRA1) (Hansford and Marshall, 2005; Hishiki et al., 1998), insulin-like growth factor 2 (IGF2)/IGF2 receptor (IGF2R) (El-Badry et al., 1991; Mohlin et al., 2013), interleukin (IL)-1β/IL-1R (Elaraj et al., 2006), IL-6/IL-6R (Ara et al., 2013; Pistoia et al., 2011), macrophage inhibitory cytokine 1 (MIC-1) (Craig et al., 2016), matrix metallopeptidases (MMPs) (Nyalendo et al., 2009; Sugiura et al., 1998), nuclear factor κB (NF-κB) (Spel et al., 2018; Zhi et al., 2014, 2015), platelet-derived growth factor receptor β (PDGFRB) (Kock et al., 2018), platelet endothelial cell adhesion molecule 1 (PECAM-1) or CD31 (Pezzolo et al., 2007), periostin (POSTN) (Sasaki et al., 2002), retinoic acid receptor responder protein 2 (RARRES2)/chemokine-like receptor 1 (CMKLR1) (Tummler et al., 2017), signal transducer and activator of transcription 3 (STAT3) (Hadjidaniel et al., 2017), transforming growth factor β1 (TGF-β1) (Castriconi et al., 2013), vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR) (Becker et al., 2010; Jakovljevic et al., 2009; Weng et al., 2017), as well as the VGF nerve growth factor inducible (Rossi et al., 1992) (Tables S1–S4). These consistent findings from analyzing the NB patient datasets reveal that the elevated EP2 expression is highly associated with the increased malignancy of NB tumors, leading us to hypothesize that PGE2 signaling via the EP2 receptor might contribute to COX activity-mediated NB growth.
Gene expression profiling reveals biological pathways responsible for phenotypic heterogeneity between UK and Sri Lankan oral squamous cell carcinomas
2015, Oral OncologyCitation Excerpt :Genes associated with tumor invasion, metastasis, and recurrence were significantly differentially expressed in UK but not Sri Lankan tumors including the upregulation of MMP3, PTGS2, LAMC2, POSTN, COL11A1, and TNC along with downregulation of DUSP1 and SLPI. Likewise, significant deregulation of other genes in Sri Lankan, but not UK tumor samples have been reported to play a role in preventing tumor invasion and metastasis (elevated expression of CD80, IL1RL1, GML, CYP27B1, SCN10A, HOXC10, and SH2D2A along with reduced expression of TWIST1, RECK, PSPH, GNG11, LSM7, and ERAP2) [20–54]. Activation of ESR1, SMAD3, and SMAD4 transcription regulators in UK tumors relative to their normal comparators might also facilitate the invasive phenotypic behavior of UK tumors [55–57].
Urine periostin as a biomarker of renal injury in chronic allograft nephropathy
2014, Transplantation ProceedingsCitation Excerpt :Currently, periostin is discussed as a major player in tissue fibrosis, but is also a critical component of mechanically challenged biological structures, including kidney tissues. Moreover, several reports describe periostin overexpression in malignant cells that had undergone EMT and metastasized [13–15]. The de novo periostin expression in the tubulointerstitium areas is most likely from myofibroblasts as described in postischemic myocardium or diseased heart valves [16].
Characterization of periostin isoform pattern in non-small cell lung cancer
2012, Lung CancerCitation Excerpt :It is present in many healthy tissues such as periodontal ligament, periosteum, cardiac valves and placenta and in tissues under mechanical stress conditions [10–16]. Its up-regulation has been observed in a wide variety of cancerous tissues, such as ovarian, breast, pancreatic, head and neck carcinomas as well as in neuroblastoma [16–21]. Periostin is thought to promote EMT of carcinoma cells by targeting the crosstalk between the epidermal growth factor receptor (EGFR) and the integrins at the plasma membrane, with consecutive activation of the Akt/PKB (protein kinase B) and the FAK (focal adhesion kinase) pathway [5,17,19,22,23].
Relevance of periostin splice variants in renal cell carcinoma
2011, American Journal of PathologyPeriostin promotes ovarian cancer angiogenesis and metastasis
2010, Gynecologic OncologyCitation Excerpt :Functionally, PN promotes the adhesion and motility of cancer cells by interacting with integrin receptors αVβ3 and αVβ5 [15]. PN overexpression also has been reported in many other human tumors including non-small cell lung cancer [16], neuroblastoma [17], breast [18], colon [19], head and neck [20], oral [21] and pancreatic cancers [22]. Upregulated PN expression or elevated PN serum levels have been reported to be correlated with tumor angiogenesis [21], metastases [19–21,23], clinical stage [24] or survival outcome [16].
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Address reprint requests to Hidefumi Sasaki, Department of Surgery II, Nagoya City University Medical School, Kawasumi 1, Mizuho-cho, Mizuho-ku, Nagoya, 467-8601, Japan.