N-Acyl Taurines are Anti-Proliferative in Prostate Cancer Cells

Endocannabinoids have been implicated in cancer development and cause heterogenous effects in tumor cells, by inducing apoptosis, reducing migration, causing anti-angiogenic activity and alterations in the cell cycle resulting in growth arrest. Recently, several novel amides of fatty acids that are...

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Published inLipids Vol. 47; no. 4; pp. 355 - 361
Main Authors Chatzakos, Vicky, Slätis, Katharina, Djureinovic, Tatjana, Helleday, Thomas, Hunt, Mary C.
Format Journal Article
LanguageEnglish
Published Berlin/Heidelberg Springer-Verlag 01.04.2012
Springer‐Verlag
Springer Nature B.V
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Abstract Endocannabinoids have been implicated in cancer development and cause heterogenous effects in tumor cells, by inducing apoptosis, reducing migration, causing anti-angiogenic activity and alterations in the cell cycle resulting in growth arrest. Recently, several novel amides of fatty acids that are structurally related to endocannabinoids have been isolated from mammalian sources, although the functions of these fatty amides are not well studied. One group of these novel fatty acid amides are the N -acyl taurines (fatty acids conjugated to the amino acid taurine). This study examined if N -acyl taurines, specifically N -arachidonoyl taurine and N -oleoyl taurine could function in a similar way to endocannabinoids and result in cell cycle alterations or growth arrest in the human prostate adenocarcinoma cell line PC-3. PC-3 cells were treated with various concentrations of N -arachidonoyl taurine and N -oleoyl taurine and cell proliferation and viability was measured using resazurin and colony formation assays. Effects of N -acyl taurines on the cell cycle was measured using FACS analysis. Treatment with N -arachidonoyl taurine and N -oleoyl taurine resulted in a significant reduction in proliferation of PC-3 cells, even at concentrations as low as 1 μM. Treatment with N -oleoyl taurine resulted in an increased number of cells in the subG1 population, suggesting apoptosis, and a lower number of cells in S-phase of the cell cycle. In summary, our results show that novel biologically active lipids, the N -acyl taurines, result in reduced proliferation in PC-3 cells.
AbstractList Endocannabinoids have been implicated in cancer development and cause heterogenous effects in tumor cells, by inducing apoptosis, reducing migration, causing anti-angiogenic activity and alterations in the cell cycle resulting in growth arrest. Recently, several novel amides of fatty acids that are structurally related to endocannabinoids have been isolated from mammalian sources, although the functions of these fatty amides are not well studied. One group of these novel fatty acid amides are the N-acyl taurines (fatty acids conjugated to the amino acid taurine). This study examined if N-acyl taurines, specifically N-arachidonoyl taurine and N-oleoyl taurine could function in a similar way to endocannabinoids and result in cell cycle alterations or growth arrest in the human prostate adenocarcinoma cell line PC-3. PC-3 cells were treated with various concentrations of N-arachidonoyl taurine and N-oleoyl taurine and cell proliferation and viability was measured using resazurin and colony formation assays. Effects of N-acyl taurines on the cell cycle was measured using FACS analysis. Treatment with N-arachidonoyl taurine and N-oleoyl taurine resulted in a significant reduction in proliferation of PC-3 cells, even at concentrations as low as 1 mu M. Treatment with N-oleoyl taurine resulted in an increased number of cells in the subG1 population, suggesting apoptosis, and a lower number of cells in S-phase of the cell cycle. In summary, our results show that novel biologically active lipids, the N-acyl taurines, result in reduced proliferation in PC-3 cells.
Endocannabinoids have been implicated in cancer development and cause heterogenous effects in tumor cells, by inducing apoptosis, reducing migration, causing anti‐angiogenic activity and alterations in the cell cycle resulting in growth arrest. Recently, several novel amides of fatty acids that are structurally related to endocannabinoids have been isolated from mammalian sources, although the functions of these fatty amides are not well studied. One group of these novel fatty acid amides are the N ‐acyl taurines (fatty acids conjugated to the amino acid taurine). This study examined if N ‐acyl taurines, specifically N ‐arachidonoyl taurine and N ‐oleoyl taurine could function in a similar way to endocannabinoids and result in cell cycle alterations or growth arrest in the human prostate adenocarcinoma cell line PC‐3. PC‐3 cells were treated with various concentrations of N ‐arachidonoyl taurine and N ‐oleoyl taurine and cell proliferation and viability was measured using resazurin and colony formation assays. Effects of N ‐acyl taurines on the cell cycle was measured using FACS analysis. Treatment with N ‐arachidonoyl taurine and N ‐oleoyl taurine resulted in a significant reduction in proliferation of PC‐3 cells, even at concentrations as low as 1 μM. Treatment with N ‐oleoyl taurine resulted in an increased number of cells in the subG1 population, suggesting apoptosis, and a lower number of cells in S‐phase of the cell cycle. In summary, our results show that novel biologically active lipids, the N ‐acyl taurines, result in reduced proliferation in PC‐3 cells.
Endocannabinoids have been implicated in cancer development and cause heterogenous effects in tumor cells, by inducing apoptosis, reducing migration, causing anti-angiogenic activity and alterations in the cell cycle resulting in growth arrest. Recently, several novel amides of fatty acids that are structurally related to endocannabinoids have been isolated from mammalian sources, although the functions of these fatty amides are not well studied. One group of these novel fatty acid amides are the N-acyl taurines (fatty acids conjugated to the amino acid taurine). This study examined if N-acyl taurines, specifically N-arachidonoyl taurine and N-oleoyl taurine could function in a similar way to endocannabinoids and result in cell cycle alterations or growth arrest in the human prostate adenocarcinoma cell line PC-3. PC-3 cells were treated with various concentrations of N-arachidonoyl taurine and N-oleoyl taurine and cell proliferation and viability was measured using resazurin and colony formation assays. Effects of N-acyl taurines on the cell cycle was measured using FACS analysis. Treatment with N-arachidonoyl taurine and N-oleoyl taurine resulted in a significant reduction in proliferation of PC-3 cells, even at concentrations as low as 1 μM. Treatment with N-oleoyl taurine resulted in an increased number of cells in the subG1 population, suggesting apoptosis, and a lower number of cells in S-phase of the cell cycle. In summary, our results show that novel biologically active lipids, the N-acyl taurines, result in reduced proliferation in PC-3 cells.[PUBLICATION ABSTRACT]
Endocannabinoids have been implicated in cancer development and cause heterogenous effects in tumor cells, by inducing apoptosis, reducing migration, causing anti‐angiogenic activity and alterations in the cell cycle resulting in growth arrest. Recently, several novel amides of fatty acids that are structurally related to endocannabinoids have been isolated from mammalian sources, although the functions of these fatty amides are not well studied. One group of these novel fatty acid amides are the N‐acyl taurines (fatty acids conjugated to the amino acid taurine). This study examined if N‐acyl taurines, specifically N‐arachidonoyl taurine and N‐oleoyl taurine could function in a similar way to endocannabinoids and result in cell cycle alterations or growth arrest in the human prostate adenocarcinoma cell line PC‐3. PC‐3 cells were treated with various concentrations of N‐arachidonoyl taurine and N‐oleoyl taurine and cell proliferation and viability was measured using resazurin and colony formation assays. Effects of N‐acyl taurines on the cell cycle was measured using FACS analysis. Treatment with N‐arachidonoyl taurine and N‐oleoyl taurine resulted in a significant reduction in proliferation of PC‐3 cells, even at concentrations as low as 1 μM. Treatment with N‐oleoyl taurine resulted in an increased number of cells in the subG1 population, suggesting apoptosis, and a lower number of cells in S‐phase of the cell cycle. In summary, our results show that novel biologically active lipids, the N‐acyl taurines, result in reduced proliferation in PC‐3 cells.
Endocannabinoids have been implicated in cancer development and cause heterogenous effects in tumor cells, by inducing apoptosis, reducing migration, causing anti-angiogenic activity and alterations in the cell cycle resulting in growth arrest. Recently, several novel amides of fatty acids that are structurally related to endocannabinoids have been isolated from mammalian sources, although the functions of these fatty amides are not well studied. One group of these novel fatty acid amides are the N-acyl taurines (fatty acids conjugated to the amino acid taurine). This study examined if N-acyl taurines, specifically N-arachidonoyl taurine and N-oleoyl taurine could function in a similar way to endocannabinoids and result in cell cycle alterations or growth arrest in the human prostate adenocarcinoma cell line PC-3. PC-3 cells were treated with various concentrations of N-arachidonoyl taurine and N-oleoyl taurine and cell proliferation and viability was measured using resazurin and colony formation assays. Effects of N-acyl taurines on the cell cycle was measured using FACS analysis. Treatment with N-arachidonoyl taurine and N-oleoyl taurine resulted in a significant reduction in proliferation of PC-3 cells, even at concentrations as low as 1 μM. Treatment with N-oleoyl taurine resulted in an increased number of cells in the subG1 population, suggesting apoptosis, and a lower number of cells in S-phase of the cell cycle. In summary, our results show that novel biologically active lipids, the N-acyl taurines, result in reduced proliferation in PC-3 cells.
Endocannabinoids have been implicated in cancer development and cause heterogenous effects in tumor cells, by inducing apoptosis, reducing migration, causing anti-angiogenic activity and alterations in the cell cycle resulting in growth arrest. Recently, several novel amides of fatty acids that are structurally related to endocannabinoids have been isolated from mammalian sources, although the functions of these fatty amides are not well studied. One group of these novel fatty acid amides are the N -acyl taurines (fatty acids conjugated to the amino acid taurine). This study examined if N -acyl taurines, specifically N -arachidonoyl taurine and N -oleoyl taurine could function in a similar way to endocannabinoids and result in cell cycle alterations or growth arrest in the human prostate adenocarcinoma cell line PC-3. PC-3 cells were treated with various concentrations of N -arachidonoyl taurine and N -oleoyl taurine and cell proliferation and viability was measured using resazurin and colony formation assays. Effects of N -acyl taurines on the cell cycle was measured using FACS analysis. Treatment with N -arachidonoyl taurine and N -oleoyl taurine resulted in a significant reduction in proliferation of PC-3 cells, even at concentrations as low as 1 μM. Treatment with N -oleoyl taurine resulted in an increased number of cells in the subG1 population, suggesting apoptosis, and a lower number of cells in S-phase of the cell cycle. In summary, our results show that novel biologically active lipids, the N -acyl taurines, result in reduced proliferation in PC-3 cells.
Author Djureinovic, Tatjana
Hunt, Mary C.
Chatzakos, Vicky
Helleday, Thomas
Slätis, Katharina
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Issue 4
Keywords Cell proliferation
Fatty acid amide hydrolase
Oleoyl taurine
Arachidonoyl taurine
PC-3 cells
Acyl amino acids
Language English
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Snippet Endocannabinoids have been implicated in cancer development and cause heterogenous effects in tumor cells, by inducing apoptosis, reducing migration, causing...
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proquest
crossref
pubmed
wiley
springer
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Aggregation Database
Index Database
Publisher
StartPage 355
SubjectTerms Adenocarcinoma - drug therapy
Adenocarcinoma - pathology
Amides
Amino acids
Apoptosis - drug effects
Arachidonic Acids - chemistry
Arachidonic Acids - pharmacology
Biomedical and Life Sciences
Cannabinoid Receptor Modulators - chemistry
Cannabinoid Receptor Modulators - pharmacology
Cell Count
Cell Cycle - drug effects
Cell Line, Tumor
Cell proliferation
Cell Proliferation - drug effects
Cell Survival - drug effects
Dose-Response Relationship, Drug
Fatty acid amide hydrolase
Fatty acids
Flow Cytometry
Humans
Life Sciences
Lipidology
Lipids
Male
Medical Biochemistry
Medicinal Chemistry
Microbial Genetics and Genomics
Molecular Genetics
molekylärgenetik
N-Acyl amino acids
N-Arachidonoyl taurine
N-Oleoyl taurine
Neurochemistry
Nutrition
Original Article
Oxazines
PC-3 cells
Prostate - drug effects
Prostate - pathology
Prostate cancer
Prostatic Neoplasms - drug therapy
Prostatic Neoplasms - pathology
Taurine - analogs & derivatives
Taurine - chemistry
Taurine - pharmacology
Xanthenes
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Title N-Acyl Taurines are Anti-Proliferative in Prostate Cancer Cells
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https://onlinelibrary.wiley.com/doi/abs/10.1007%2Fs11745-011-3639-9
https://www.ncbi.nlm.nih.gov/pubmed/22160494
https://www.proquest.com/docview/938670416
https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-76070
https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-173322
Volume 47
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