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 in | Lipids Vol. 47; no. 4; pp. 355 - 361 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Berlin/Heidelberg
Springer-Verlag
01.04.2012
Springer‐Verlag Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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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 |
Author_xml | – sequence: 1 givenname: Vicky surname: Chatzakos fullname: Chatzakos, Vicky organization: Department of Genetics, Microbiology and Toxicology, Stockholm University – sequence: 2 givenname: Katharina surname: Slätis fullname: Slätis, Katharina organization: Department of Genetics, Microbiology and Toxicology, Stockholm University – sequence: 3 givenname: Tatjana surname: Djureinovic fullname: Djureinovic, Tatjana organization: Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University – sequence: 4 givenname: Thomas surname: Helleday fullname: Helleday, Thomas organization: Department of Genetics, Microbiology and Toxicology, Stockholm University – sequence: 5 givenname: Mary C. surname: Hunt fullname: Hunt, Mary C. email: mary.hunt@dit.ie organization: School of Biological Sciences, Dublin Institute of Technology |
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Keywords | Cell proliferation Fatty acid amide hydrolase Oleoyl taurine Arachidonoyl taurine PC-3 cells Acyl amino acids |
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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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