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Title:
CD38 is methylated in prostate cancer and regulates extracellular NAD+ | Cancer & Metabolism
Description:
Background Cancer cell metabolism requires sustained pools of intracellular nicotinamide adenine dinucleotide (NAD+) which is maintained by a balance of NAD+ hydrolase activity and NAD+ salvage activity. We recently reported that human prostate cancer can be initiated following oncogene expression in progenitor-like luminal cells marked by low expression of the NAD+-consuming enzyme CD38. CD38 expression is reduced in prostate cancer compared to benign prostate, suggesting that tumor cells may reduce CD38 expression in order to enhance pools of NAD+. However, little is known about how CD38 expression is repressed in advanced prostate cancer and whether CD38 plays a role in regulating NAD+ levels in prostate epithelial cells. Methods CD38 expression, its association with recurrence after prostatectomy for clinically localized prostate cancer, and DNA methylation of the CD38 promoter were evaluated in human prostate tissues representing various stages of disease progression. CD38 was inducibly over-expressed in benign and malignant human prostate cell lines in order to determine the effects on cell proliferation and levels of NAD+ and NADH. NAD+ and NADH were also measured in urogenital tissues from wild-type and CD38 knockout mice. Results CD38 mRNA expression was reduced in metastatic castration-resistant prostate cancer compared to localized prostate cancer. In a large cohort of men undergoing radical prostatectomy, CD38 protein expression was inversely correlated with recurrence. We identified methylation of the CD38 promoter in primary and metastatic prostate cancer. Over-expression of wild-type CD38, but not an NAD+ hydrolase-deficient mutant, depleted extracellular NAD+ levels in benign and malignant prostate cell lines. However, expression of CD38 did not significantly alter intracellular NAD+ levels in human prostate cell lines grown in vitro and in urogenital tissues isolated from wild-type and CD38 knockout mice. Conclusions CD38 protein expression in prostate cancer is associated with risk of recurrence. Methylation results suggest that CD38 is epigenetically regulated in localized and metastatic prostate cancer tissues. Our study provides support for CD38 as a regulator of extracellular, but not intracellular, NAD+ in epithelial cells. These findings suggest that repression of CD38 by methylation may serve to increase the availability of extracellular NAD+ in prostate cancer tissues.
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Keywords {🔍}
nad, prostate, cancer, cells, cell, expression, levels, article, google, scholar, cas, methylation, dna, tissues, tissue, wildtype, additional, file, extracellular, intracellular, seminal, min, fig, media, mice, shown, human, measured, knockout, lines, usa, analysis, samples, relative, dox, proliferation, lncap, vesicle, benign, recurrence, nadh, protein, primary, sem, data, total, medicine, los, angeles, epithelial,
Topics {✒️}
ecto-nicotinamide adenine dinucleotide hedgehog-dependent tumor-initiating cells beta-nicotinamide adenine dinucleotide amplified full-length cd38 locus-specific methylation levels androgen-receptor signaling axis snail promotes resistance cyclic adp-ribose catalyzed nad+/nadh-glo assay normalized methylation-sensitive restriction enzymes epithelial markers p-cadherin poly-adp-ribose polymerases castration-resistant prostate cancer unbound mbd2-mbd polypeptides identify cpg methylation mutafova-yambolieva vn nad+/nadh-glo assay 30 min article download pdf cells expressing wild-type human leukocyte antigen-dr dictate potential immune-suppressing percoll-purified seminal vesicle nad+-consuming enzyme cd38 fluorescence-activated cell sorting cd38/adp-ribosyl cyclase sequence alignment/map format quantitative real-time pcr nad+/nadh-glo assay wild-type mouse prostate humanized cd38-targeting antibody nad+-induced cell death primary prostate cancers nad+ hydrolase-deficient mutant nicotinamide adenine dinucleotide mutant cd38-expressing cells clinically localized disease full access androgen receptor activity 300 mm tris-base +160mmnaoh mbd2-mbd-coated beads methylated-dna precipitation assay nad+/nadh cycling assay cancer/benign biopsy cores subsequent compare-ms experiments intracellular/extracellular nad+ levels related subjects cyclic adp ribose shrna-mediated knockdown mesenchymal markers desmin de la iglesia-vicente
Questions {❓}
- Several key questions remain unanswered, including (1) What is the level of CD38 expression in metastatic castration-resistant prostate cancer?
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mainEntity:
headline:CD38 is methylated in prostate cancer and regulates extracellular NAD+
description:Cancer cell metabolism requires sustained pools of intracellular nicotinamide adenine dinucleotide (NAD+) which is maintained by a balance of NAD+ hydrolase activity and NAD+ salvage activity. We recently reported that human prostate cancer can be initiated following oncogene expression in progenitor-like luminal cells marked by low expression of the NAD+-consuming enzyme CD38. CD38 expression is reduced in prostate cancer compared to benign prostate, suggesting that tumor cells may reduce CD38 expression in order to enhance pools of NAD+. However, little is known about how CD38 expression is repressed in advanced prostate cancer and whether CD38 plays a role in regulating NAD+ levels in prostate epithelial cells. CD38 expression, its association with recurrence after prostatectomy for clinically localized prostate cancer, and DNA methylation of the CD38 promoter were evaluated in human prostate tissues representing various stages of disease progression. CD38 was inducibly over-expressed in benign and malignant human prostate cell lines in order to determine the effects on cell proliferation and levels of NAD+ and NADH. NAD+ and NADH were also measured in urogenital tissues from wild-type and CD38 knockout mice. CD38 mRNA expression was reduced in metastatic castration-resistant prostate cancer compared to localized prostate cancer. In a large cohort of men undergoing radical prostatectomy, CD38 protein expression was inversely correlated with recurrence. We identified methylation of the CD38 promoter in primary and metastatic prostate cancer. Over-expression of wild-type CD38, but not an NAD+ hydrolase-deficient mutant, depleted extracellular NAD+ levels in benign and malignant prostate cell lines. However, expression of CD38 did not significantly alter intracellular NAD+ levels in human prostate cell lines grown in vitro and in urogenital tissues isolated from wild-type and CD38 knockout mice. CD38 protein expression in prostate cancer is associated with risk of recurrence. Methylation results suggest that CD38 is epigenetically regulated in localized and metastatic prostate cancer tissues. Our study provides support for CD38 as a regulator of extracellular, but not intracellular, NAD+ in epithelial cells. These findings suggest that repression of CD38 by methylation may serve to increase the availability of extracellular NAD+ in prostate cancer tissues.
datePublished:2018-09-21T00:00:00Z
dateModified:2018-09-21T00:00:00Z
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keywords:
Prostate
CD38
NAD+
Methylation
Cancer Research
Oncology
Metabolomics
Metabolic Diseases
Imaging / Radiology
Cell Biology
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headline:CD38 is methylated in prostate cancer and regulates extracellular NAD+
description:Cancer cell metabolism requires sustained pools of intracellular nicotinamide adenine dinucleotide (NAD+) which is maintained by a balance of NAD+ hydrolase activity and NAD+ salvage activity. We recently reported that human prostate cancer can be initiated following oncogene expression in progenitor-like luminal cells marked by low expression of the NAD+-consuming enzyme CD38. CD38 expression is reduced in prostate cancer compared to benign prostate, suggesting that tumor cells may reduce CD38 expression in order to enhance pools of NAD+. However, little is known about how CD38 expression is repressed in advanced prostate cancer and whether CD38 plays a role in regulating NAD+ levels in prostate epithelial cells. CD38 expression, its association with recurrence after prostatectomy for clinically localized prostate cancer, and DNA methylation of the CD38 promoter were evaluated in human prostate tissues representing various stages of disease progression. CD38 was inducibly over-expressed in benign and malignant human prostate cell lines in order to determine the effects on cell proliferation and levels of NAD+ and NADH. NAD+ and NADH were also measured in urogenital tissues from wild-type and CD38 knockout mice. CD38 mRNA expression was reduced in metastatic castration-resistant prostate cancer compared to localized prostate cancer. In a large cohort of men undergoing radical prostatectomy, CD38 protein expression was inversely correlated with recurrence. We identified methylation of the CD38 promoter in primary and metastatic prostate cancer. Over-expression of wild-type CD38, but not an NAD+ hydrolase-deficient mutant, depleted extracellular NAD+ levels in benign and malignant prostate cell lines. However, expression of CD38 did not significantly alter intracellular NAD+ levels in human prostate cell lines grown in vitro and in urogenital tissues isolated from wild-type and CD38 knockout mice. CD38 protein expression in prostate cancer is associated with risk of recurrence. Methylation results suggest that CD38 is epigenetically regulated in localized and metastatic prostate cancer tissues. Our study provides support for CD38 as a regulator of extracellular, but not intracellular, NAD+ in epithelial cells. These findings suggest that repression of CD38 by methylation may serve to increase the availability of extracellular NAD+ in prostate cancer tissues.
datePublished:2018-09-21T00:00:00Z
dateModified:2018-09-21T00:00:00Z
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pageEnd:17
license:http://creativecommons.org/publicdomain/zero/1.0/
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keywords:
Prostate
CD38
NAD+
Methylation
Cancer Research
Oncology
Metabolomics
Metabolic Diseases
Imaging / Radiology
Cell Biology
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