2011
DOI: 10.1002/pros.21471
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Abstract: Background Nonsteroidal anti-inflammatory drug-activated gene (NAG-1), a divergent member of the transforming growth factor beta superfamily, has been implicated in many cellular processes, including inflammation, early bone formation, apoptosis, and tumorigenesis. Recent clinical studies suggests that a C to G single nucleotide polymorphism at position 6 (histidine to aspartic acid substitution, or H6D) of the NAG-1 protein is associated with lower human prostate cancer incidence. The objective of the current… Show more

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Cited by 18 publications
(25 citation statements)
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“…Because sufficient hNAG-1 protein is not available, tumor xenografts with stably transduced B16–F10 melanoma cells expressing hNAG-1 was used as a tool to increase serum levels of hNAG-1 in obese C57BL/6 mice as previously reported with nude mice (2425). B16–F10 melanoma cells expressing only vector served as the control.…”
Section: Resultsmentioning
confidence: 99%
“…Because sufficient hNAG-1 protein is not available, tumor xenografts with stably transduced B16–F10 melanoma cells expressing hNAG-1 was used as a tool to increase serum levels of hNAG-1 in obese C57BL/6 mice as previously reported with nude mice (2425). B16–F10 melanoma cells expressing only vector served as the control.…”
Section: Resultsmentioning
confidence: 99%
“…In athymic nude mice inoculated with DU145 PCa cells transfected with appropriate coding sequences, the H6D variant clearly interfered with tumor development by lowering levels of cyclin D1 and IGF-1 in the serum resulting in smaller tumors than in controls with wild-type GDF-15. 90 However, the systemic role for body-weight regulation and the induction of tumor associated cachexia is likely not compromised in the H6D variant compared with wild-type GDF-15, as both proteins significantly reduce the amount of abdominal fat in experimental mice and reduce adipose tissue signaling. 90 A common problem associated with long-term PCa therapy is the development of hormone refractory PCa and resistance to chemotherapy.…”
Section: Gdf-15 In Pcamentioning
confidence: 99%
“…90 However, the systemic role for body-weight regulation and the induction of tumor associated cachexia is likely not compromised in the H6D variant compared with wild-type GDF-15, as both proteins significantly reduce the amount of abdominal fat in experimental mice and reduce adipose tissue signaling. 90 A common problem associated with long-term PCa therapy is the development of hormone refractory PCa and resistance to chemotherapy. It is estimated that about 50% of patients treated by first-line castration do not respond to second-line of chemotherapy with Docetaxel.…”
Section: Gdf-15 In Pcamentioning
confidence: 99%
“…Five genes known to contain an ARE in the proximal promoter (IL-32, HMOX1, GDF15, BHLHE40, and TMPRSS2, see Supplemental Table 3) were examined to determine whether FlnA16-24 affected their transcription (Figure 7D). The expression of growth differentiation factor 15 (GDF15), a member of the transforming growth factor beta (TGFβ) superfamily, and interleukin-32 (IL-32), is known to induce apoptosis (Park, et al 2012; Podar, et al 2007; Wang, et al 2012; Yun, et al 2013), while TMPRSS2 is a known AR target suppressed in CRPC. Heme oxygenase 1 (HMOX1) counteracts oxidative and inflammatory damage and is implicated in the adhesive and morphological properties of tumor cells (Gueron, et al 2014), while Basic loop-helix-loop E40 (BHLHE40) is a transcription factor is involved in the regulation of cell differentiation, response to hypoxia and carcinogenesis (Wu, et al 2014).…”
Section: Resultsmentioning
confidence: 99%
“…Previous studies showed that TMPRSS2 mRNA expression, but not TMPRSS2-ERG gene fusion, is decreased in CRPC, since the gene fusion likely cause an increase in ERG expression instead of TMPRSS2 (Cai, et al 2009). FlnA also upregulates two other genes, GDF15 and IL-32 that are also associated with increased apoptosis (Park et al 2012; Wang et al 2012; Yun et al 2013). Therefore, it is likely that nuclear FlnA induces apoptosis by increasing GDF-15 and IL-32 levels.…”
Section: Discussionmentioning
confidence: 99%