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    • Placental growth factor PlGF is an angiogenic

    2018-11-06

    Placental growth factor (PlGF) is an angiogenic protein often highly upregulated in solid tumors contributing to their growth and survival (Kim et al., 2012). PlGF can promote angiogenesis either by directly stimulating endothelial cell growth or by recruiting pro-angiogenic cell types. Of the two main human PlGF isoforms, PlGF1 and PlGF2, only PlGF2 has the exclusive ability to bind heparin and neuropilin receptors. Elevated circulating PlGF in neuroendocrine tumors correlates with advanced tumor grading and reduced patient survival (Hilfenhaus et al., 2013). Studies also suggest that PlGF2 may promote dorsal root ganglion survival and prevent neurite collapse (Cheng et al., 2004), thus providing an additional role for this growth factor in cell survival. Of the four PlGFs, PlGF2 appears to bind to the most diverse number of receptors, including VEGFR-1, HSPG, NRP-1, and NRP-2 (De Falco, 2012). Previous studies have shown that neurotrophins, through their cognate receptors, regulate the proliferation, survival, and differentiation of neural crest GDC0941 as well as CNS neuro-epithelial precursors (Huang and Reichardt, 2001). Numerous studies have examined their presence and role in neuroblastoma (Nakagawara et al., 1994; Brodeur et al., 1997; Jaboin et al., 2002; Nakamura et al., 2006; Dominici et al., 1997; Aoyama et al., 2001; Hecht et al., 2005; Ho et al., 2002), including studies which show the roles of NTRs in survival, invasiveness, and chemoresistance. In the present study, we show that both TRKB and LNGFR were significantly higher in neuroblastoma stem cells when compared to the two other predominant cell types. This suggests that the increased survival, proliferation, invasiveness, and resistance seen in neuroblastoma tumors were mediated by the stem cell subpopulation.
    Acknowledgments This research was supported in part by grants from the National Cancer Institute (CA 77593). This paper is dedicated to Dr. June L. Biedler and Barbara A. Spengler, who initiated the research on phenotypic plasticity in human neuroblastoma cells.
    Introduction Genomic imprinting is an epigenetic phenomenon characterized by parental origin-dependent expression of the imprinted genes (Barlow and Bartolomei, 2014; Bartolomei and Ferguson-Smith, 2011; Lawson et al., 2013; Li, 2013; Peters, 2014; Tomizawa and Sasaki, 2012). Roughly 150 imprinted genes have been identified in mouse and many of them are conserved in humans (Barlow and Bartolomei, 2014; Bartolomei and Ferguson-Smith, 2011; Kelsey and Bartolomei, 2012). A large number of the imprinted genes are clustered and co-regulated by a cis-acting imprinting control region called ICR (Ben-Porath and Cedar, 2000; Lewis and Reik, 2006; Robertson, 2005). ICRs are marked by germline-derived differential DNA methylation that is present at the CpG sites within the ICR of either paternal chromosome or maternal chromosome (Barlow and Bartolomei, 2014; Bartolomei and Ferguson-Smith, 2011; Ciccone et al., 2009). Allelic differential DNA methylation at the ICRs is maintained by DNA methyltransferase complexes to prevent its loss during cell divisions (Li et al., 1993; Li and Zhang, 2014; Moore et al., 2013; Reik et al., 2001; Tomizawa and Sasaki, 2012). Without DNA methyltransferase complexes, the newly synthesized DNA will lack DNA methylation at the CpG sites including those at the ICRs (Kaneda et al., 2004; Klose and Bird, 2006; Law and Jacobsen, 2010; Li and Zhang, 2014; Okano et al., 1999). ZFP57 and PGC7/Stella are two maternal-effect genes necessary for the maintenance of DNA methylation imprint at most imprinted regions examined (Li et al., 2008; Mackay et al., 2008; Nakamura et al., 2007; Payer et al., 2003; Quenneville et al., 2011; Strogantsev et al., 2015). Human and mouse ZFP57 proteins appear to play similar roles in genomic imprinting (Mackay et al., 2008; Takikawa et al., 2013b). Our previous studies have demonstrated that ZFP57 interacts with DNA methyltranferases via its cofactor KAP1/TRIM28 (Li et al., 2008; Zuo et al., 2012). Indeed, KAP1/TRIM28 also appears to be required for the maintenance of DNA methylation imprint (Messerschmidt et al., 2012; Zuo et al., 2012). Therefore, the DNA methyltransferase complexes containing ZFP57 and KAP1/TRIM28 play a major role in maintaining DNA methylation imprint (Li, 2010, 2013).