Benzylidenetetralones, cyclic chalcone analogues, induce cell cycle arrest and apoptosis in HCT116 colorectal cancer cells

Abstract Colorectal cancer is the third most common cancer in the world, with 1.2 million new cancer cases annually. Chalcones are secondary metabolite precursors of flavonoids that exhibit diverse biological activities, including antioxidant and antitumor activities. The aim of this study was to in...
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Autor*in:	Drutovic, David [verfasserIn] Chripkova, Martina Pilatova, Martina Kruzliak, Peter Perjesi, Pal Sarissky, Marek Lupi, Monica Damia, Giovanna Broggini, Massimo Mojzis, Jan

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	Benzylidenetetralones Cyclic chalcone analogues Cell cycle arrest Apoptosis Colorectal cancer cells

Anmerkung:	© International Society of Oncology and BioMarkers (ISOBM) 2014

Übergeordnetes Werk:	Enthalten in: Tumor biology - Amsterdam : IOS Press, 1987, 35(2014), 10 vom: 10. Juli, Seite 9967-9975
Übergeordnetes Werk:	volume:35 ; year:2014 ; number:10 ; day:10 ; month:07 ; pages:9967-9975

Links:	Volltext

DOI / URN:	10.1007/s13277-014-2289-y

Katalog-ID:	SPR031133746

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100	1		\|a Drutovic, David \|e verfasserin \|4 aut
245	1	0	\|a Benzylidenetetralones, cyclic chalcone analogues, induce cell cycle arrest and apoptosis in HCT116 colorectal cancer cells
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520			\|a Abstract Colorectal cancer is the third most common cancer in the world, with 1.2 million new cancer cases annually. Chalcones are secondary metabolite precursors of flavonoids that exhibit diverse biological activities, including antioxidant and antitumor activities. The aim of this study was to investigate the antiproliferative effect of new synthetic chalcone derivatives on HCT116 cells. (E)-2-(2′,4′-dimethoxybenzylidene)-1-tetralone (Q705) was found to be the most active ($ IC_{50} $ = 3.44 ± 0.25 μM). Based on these results, this compound was chosen for further analysis of its biochemical and molecular mechanisms. Our results showed that Q705 inhibited the growth and clonogenicity of HCT116 cells. The results of a flow cytometric analyses suggested that this compound caused a significant cell cycle arrest in G2/M phase and increased the proportion of cells in the subG0/G1 phase, marker of apoptosis. Q705-induced apoptosis was confirmed by TdT-mediated dUTP nick end labelling (TUNEL) assay. Treatment of HCT116 cells with this chalcone significantly increased the caspase-3,-7 activity and resulted in cleavage of poly-ADP-ribose polymerase (PARP). Changes in the nuclear morphology such as chromatin condensation were also observed. These effects were associated with a decreased expression of bcl-$ x_{L} $ and increased overall ratio of bax/bcl-$ x_{L} $ mRNA levels. Immunofluorescence and qRT-PCR analysis revealed that Q705 induced H2AX histone modifications characteristic of DNA damage, disruption of microtubule organization and downregulation of tubulins. In summary, these results suggest that the cyclic chalcone analogue Q705 has potential as a new compound for colorectal cancer therapy.
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650		4	\|a Cell cycle arrest \|7 (dpeaa)DE-He213
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700	1		\|a Chripkova, Martina \|4 aut
700	1		\|a Pilatova, Martina \|4 aut
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700	1		\|a Sarissky, Marek \|4 aut
700	1		\|a Lupi, Monica \|4 aut
700	1		\|a Damia, Giovanna \|4 aut
700	1		\|a Broggini, Massimo \|4 aut
700	1		\|a Mojzis, Jan \|4 aut
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allfields	10.1007/s13277-014-2289-y doi (DE-627)SPR031133746 (SPR)s13277-014-2289-y-e DE-627 ger DE-627 rakwb eng Drutovic, David verfasserin aut Benzylidenetetralones, cyclic chalcone analogues, induce cell cycle arrest and apoptosis in HCT116 colorectal cancer cells 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2014 Abstract Colorectal cancer is the third most common cancer in the world, with 1.2 million new cancer cases annually. Chalcones are secondary metabolite precursors of flavonoids that exhibit diverse biological activities, including antioxidant and antitumor activities. The aim of this study was to investigate the antiproliferative effect of new synthetic chalcone derivatives on HCT116 cells. (E)-2-(2′,4′-dimethoxybenzylidene)-1-tetralone (Q705) was found to be the most active ($ IC_{50} $ = 3.44 ± 0.25 μM). Based on these results, this compound was chosen for further analysis of its biochemical and molecular mechanisms. Our results showed that Q705 inhibited the growth and clonogenicity of HCT116 cells. The results of a flow cytometric analyses suggested that this compound caused a significant cell cycle arrest in G2/M phase and increased the proportion of cells in the subG0/G1 phase, marker of apoptosis. Q705-induced apoptosis was confirmed by TdT-mediated dUTP nick end labelling (TUNEL) assay. Treatment of HCT116 cells with this chalcone significantly increased the caspase-3,-7 activity and resulted in cleavage of poly-ADP-ribose polymerase (PARP). Changes in the nuclear morphology such as chromatin condensation were also observed. These effects were associated with a decreased expression of bcl-$ x_{L} $ and increased overall ratio of bax/bcl-$ x_{L} $ mRNA levels. Immunofluorescence and qRT-PCR analysis revealed that Q705 induced H2AX histone modifications characteristic of DNA damage, disruption of microtubule organization and downregulation of tubulins. In summary, these results suggest that the cyclic chalcone analogue Q705 has potential as a new compound for colorectal cancer therapy. Benzylidenetetralones (dpeaa)DE-He213 Cyclic chalcone analogues (dpeaa)DE-He213 Cell cycle arrest (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Colorectal cancer cells (dpeaa)DE-He213 Chripkova, Martina aut Pilatova, Martina aut Kruzliak, Peter aut Perjesi, Pal aut Sarissky, Marek aut Lupi, Monica aut Damia, Giovanna aut Broggini, Massimo aut Mojzis, Jan aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 35(2014), 10 vom: 10. Juli, Seite 9967-9975 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:35 year:2014 number:10 day:10 month:07 pages:9967-9975 https://dx.doi.org/10.1007/s13277-014-2289-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_187 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 35 2014 10 10 07 9967-9975
spelling	10.1007/s13277-014-2289-y doi (DE-627)SPR031133746 (SPR)s13277-014-2289-y-e DE-627 ger DE-627 rakwb eng Drutovic, David verfasserin aut Benzylidenetetralones, cyclic chalcone analogues, induce cell cycle arrest and apoptosis in HCT116 colorectal cancer cells 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2014 Abstract Colorectal cancer is the third most common cancer in the world, with 1.2 million new cancer cases annually. Chalcones are secondary metabolite precursors of flavonoids that exhibit diverse biological activities, including antioxidant and antitumor activities. The aim of this study was to investigate the antiproliferative effect of new synthetic chalcone derivatives on HCT116 cells. (E)-2-(2′,4′-dimethoxybenzylidene)-1-tetralone (Q705) was found to be the most active ($ IC_{50} $ = 3.44 ± 0.25 μM). Based on these results, this compound was chosen for further analysis of its biochemical and molecular mechanisms. Our results showed that Q705 inhibited the growth and clonogenicity of HCT116 cells. The results of a flow cytometric analyses suggested that this compound caused a significant cell cycle arrest in G2/M phase and increased the proportion of cells in the subG0/G1 phase, marker of apoptosis. Q705-induced apoptosis was confirmed by TdT-mediated dUTP nick end labelling (TUNEL) assay. Treatment of HCT116 cells with this chalcone significantly increased the caspase-3,-7 activity and resulted in cleavage of poly-ADP-ribose polymerase (PARP). Changes in the nuclear morphology such as chromatin condensation were also observed. These effects were associated with a decreased expression of bcl-$ x_{L} $ and increased overall ratio of bax/bcl-$ x_{L} $ mRNA levels. Immunofluorescence and qRT-PCR analysis revealed that Q705 induced H2AX histone modifications characteristic of DNA damage, disruption of microtubule organization and downregulation of tubulins. In summary, these results suggest that the cyclic chalcone analogue Q705 has potential as a new compound for colorectal cancer therapy. Benzylidenetetralones (dpeaa)DE-He213 Cyclic chalcone analogues (dpeaa)DE-He213 Cell cycle arrest (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Colorectal cancer cells (dpeaa)DE-He213 Chripkova, Martina aut Pilatova, Martina aut Kruzliak, Peter aut Perjesi, Pal aut Sarissky, Marek aut Lupi, Monica aut Damia, Giovanna aut Broggini, Massimo aut Mojzis, Jan aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 35(2014), 10 vom: 10. Juli, Seite 9967-9975 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:35 year:2014 number:10 day:10 month:07 pages:9967-9975 https://dx.doi.org/10.1007/s13277-014-2289-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_187 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 35 2014 10 10 07 9967-9975
allfields_unstemmed	10.1007/s13277-014-2289-y doi (DE-627)SPR031133746 (SPR)s13277-014-2289-y-e DE-627 ger DE-627 rakwb eng Drutovic, David verfasserin aut Benzylidenetetralones, cyclic chalcone analogues, induce cell cycle arrest and apoptosis in HCT116 colorectal cancer cells 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2014 Abstract Colorectal cancer is the third most common cancer in the world, with 1.2 million new cancer cases annually. Chalcones are secondary metabolite precursors of flavonoids that exhibit diverse biological activities, including antioxidant and antitumor activities. The aim of this study was to investigate the antiproliferative effect of new synthetic chalcone derivatives on HCT116 cells. (E)-2-(2′,4′-dimethoxybenzylidene)-1-tetralone (Q705) was found to be the most active ($ IC_{50} $ = 3.44 ± 0.25 μM). Based on these results, this compound was chosen for further analysis of its biochemical and molecular mechanisms. Our results showed that Q705 inhibited the growth and clonogenicity of HCT116 cells. The results of a flow cytometric analyses suggested that this compound caused a significant cell cycle arrest in G2/M phase and increased the proportion of cells in the subG0/G1 phase, marker of apoptosis. Q705-induced apoptosis was confirmed by TdT-mediated dUTP nick end labelling (TUNEL) assay. Treatment of HCT116 cells with this chalcone significantly increased the caspase-3,-7 activity and resulted in cleavage of poly-ADP-ribose polymerase (PARP). Changes in the nuclear morphology such as chromatin condensation were also observed. These effects were associated with a decreased expression of bcl-$ x_{L} $ and increased overall ratio of bax/bcl-$ x_{L} $ mRNA levels. Immunofluorescence and qRT-PCR analysis revealed that Q705 induced H2AX histone modifications characteristic of DNA damage, disruption of microtubule organization and downregulation of tubulins. In summary, these results suggest that the cyclic chalcone analogue Q705 has potential as a new compound for colorectal cancer therapy. Benzylidenetetralones (dpeaa)DE-He213 Cyclic chalcone analogues (dpeaa)DE-He213 Cell cycle arrest (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Colorectal cancer cells (dpeaa)DE-He213 Chripkova, Martina aut Pilatova, Martina aut Kruzliak, Peter aut Perjesi, Pal aut Sarissky, Marek aut Lupi, Monica aut Damia, Giovanna aut Broggini, Massimo aut Mojzis, Jan aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 35(2014), 10 vom: 10. Juli, Seite 9967-9975 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:35 year:2014 number:10 day:10 month:07 pages:9967-9975 https://dx.doi.org/10.1007/s13277-014-2289-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_187 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 35 2014 10 10 07 9967-9975
allfieldsGer	10.1007/s13277-014-2289-y doi (DE-627)SPR031133746 (SPR)s13277-014-2289-y-e DE-627 ger DE-627 rakwb eng Drutovic, David verfasserin aut Benzylidenetetralones, cyclic chalcone analogues, induce cell cycle arrest and apoptosis in HCT116 colorectal cancer cells 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2014 Abstract Colorectal cancer is the third most common cancer in the world, with 1.2 million new cancer cases annually. Chalcones are secondary metabolite precursors of flavonoids that exhibit diverse biological activities, including antioxidant and antitumor activities. The aim of this study was to investigate the antiproliferative effect of new synthetic chalcone derivatives on HCT116 cells. (E)-2-(2′,4′-dimethoxybenzylidene)-1-tetralone (Q705) was found to be the most active ($ IC_{50} $ = 3.44 ± 0.25 μM). Based on these results, this compound was chosen for further analysis of its biochemical and molecular mechanisms. Our results showed that Q705 inhibited the growth and clonogenicity of HCT116 cells. The results of a flow cytometric analyses suggested that this compound caused a significant cell cycle arrest in G2/M phase and increased the proportion of cells in the subG0/G1 phase, marker of apoptosis. Q705-induced apoptosis was confirmed by TdT-mediated dUTP nick end labelling (TUNEL) assay. Treatment of HCT116 cells with this chalcone significantly increased the caspase-3,-7 activity and resulted in cleavage of poly-ADP-ribose polymerase (PARP). Changes in the nuclear morphology such as chromatin condensation were also observed. These effects were associated with a decreased expression of bcl-$ x_{L} $ and increased overall ratio of bax/bcl-$ x_{L} $ mRNA levels. Immunofluorescence and qRT-PCR analysis revealed that Q705 induced H2AX histone modifications characteristic of DNA damage, disruption of microtubule organization and downregulation of tubulins. In summary, these results suggest that the cyclic chalcone analogue Q705 has potential as a new compound for colorectal cancer therapy. Benzylidenetetralones (dpeaa)DE-He213 Cyclic chalcone analogues (dpeaa)DE-He213 Cell cycle arrest (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Colorectal cancer cells (dpeaa)DE-He213 Chripkova, Martina aut Pilatova, Martina aut Kruzliak, Peter aut Perjesi, Pal aut Sarissky, Marek aut Lupi, Monica aut Damia, Giovanna aut Broggini, Massimo aut Mojzis, Jan aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 35(2014), 10 vom: 10. Juli, Seite 9967-9975 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:35 year:2014 number:10 day:10 month:07 pages:9967-9975 https://dx.doi.org/10.1007/s13277-014-2289-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_187 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 35 2014 10 10 07 9967-9975
allfieldsSound	10.1007/s13277-014-2289-y doi (DE-627)SPR031133746 (SPR)s13277-014-2289-y-e DE-627 ger DE-627 rakwb eng Drutovic, David verfasserin aut Benzylidenetetralones, cyclic chalcone analogues, induce cell cycle arrest and apoptosis in HCT116 colorectal cancer cells 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2014 Abstract Colorectal cancer is the third most common cancer in the world, with 1.2 million new cancer cases annually. Chalcones are secondary metabolite precursors of flavonoids that exhibit diverse biological activities, including antioxidant and antitumor activities. The aim of this study was to investigate the antiproliferative effect of new synthetic chalcone derivatives on HCT116 cells. (E)-2-(2′,4′-dimethoxybenzylidene)-1-tetralone (Q705) was found to be the most active ($ IC_{50} $ = 3.44 ± 0.25 μM). Based on these results, this compound was chosen for further analysis of its biochemical and molecular mechanisms. Our results showed that Q705 inhibited the growth and clonogenicity of HCT116 cells. The results of a flow cytometric analyses suggested that this compound caused a significant cell cycle arrest in G2/M phase and increased the proportion of cells in the subG0/G1 phase, marker of apoptosis. Q705-induced apoptosis was confirmed by TdT-mediated dUTP nick end labelling (TUNEL) assay. Treatment of HCT116 cells with this chalcone significantly increased the caspase-3,-7 activity and resulted in cleavage of poly-ADP-ribose polymerase (PARP). Changes in the nuclear morphology such as chromatin condensation were also observed. These effects were associated with a decreased expression of bcl-$ x_{L} $ and increased overall ratio of bax/bcl-$ x_{L} $ mRNA levels. Immunofluorescence and qRT-PCR analysis revealed that Q705 induced H2AX histone modifications characteristic of DNA damage, disruption of microtubule organization and downregulation of tubulins. In summary, these results suggest that the cyclic chalcone analogue Q705 has potential as a new compound for colorectal cancer therapy. Benzylidenetetralones (dpeaa)DE-He213 Cyclic chalcone analogues (dpeaa)DE-He213 Cell cycle arrest (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Colorectal cancer cells (dpeaa)DE-He213 Chripkova, Martina aut Pilatova, Martina aut Kruzliak, Peter aut Perjesi, Pal aut Sarissky, Marek aut Lupi, Monica aut Damia, Giovanna aut Broggini, Massimo aut Mojzis, Jan aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 35(2014), 10 vom: 10. Juli, Seite 9967-9975 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:35 year:2014 number:10 day:10 month:07 pages:9967-9975 https://dx.doi.org/10.1007/s13277-014-2289-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_187 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 35 2014 10 10 07 9967-9975
language	English
source	Enthalten in Tumor biology 35(2014), 10 vom: 10. Juli, Seite 9967-9975 volume:35 year:2014 number:10 day:10 month:07 pages:9967-9975
sourceStr	Enthalten in Tumor biology 35(2014), 10 vom: 10. Juli, Seite 9967-9975 volume:35 year:2014 number:10 day:10 month:07 pages:9967-9975
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Benzylidenetetralones Cyclic chalcone analogues Cell cycle arrest Apoptosis Colorectal cancer cells
isfreeaccess_bool	false
container_title	Tumor biology
authorswithroles_txt_mv	Drutovic, David @@aut@@ Chripkova, Martina @@aut@@ Pilatova, Martina @@aut@@ Kruzliak, Peter @@aut@@ Perjesi, Pal @@aut@@ Sarissky, Marek @@aut@@ Lupi, Monica @@aut@@ Damia, Giovanna @@aut@@ Broggini, Massimo @@aut@@ Mojzis, Jan @@aut@@
publishDateDaySort_date	2014-07-10T00:00:00Z
hierarchy_top_id	300897855
id	SPR031133746
language_de	englisch
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author	Drutovic, David
spellingShingle	Drutovic, David misc Benzylidenetetralones misc Cyclic chalcone analogues misc Cell cycle arrest misc Apoptosis misc Colorectal cancer cells Benzylidenetetralones, cyclic chalcone analogues, induce cell cycle arrest and apoptosis in HCT116 colorectal cancer cells
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topic_title	Benzylidenetetralones, cyclic chalcone analogues, induce cell cycle arrest and apoptosis in HCT116 colorectal cancer cells Benzylidenetetralones (dpeaa)DE-He213 Cyclic chalcone analogues (dpeaa)DE-He213 Cell cycle arrest (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Colorectal cancer cells (dpeaa)DE-He213
topic	misc Benzylidenetetralones misc Cyclic chalcone analogues misc Cell cycle arrest misc Apoptosis misc Colorectal cancer cells
topic_unstemmed	misc Benzylidenetetralones misc Cyclic chalcone analogues misc Cell cycle arrest misc Apoptosis misc Colorectal cancer cells
topic_browse	misc Benzylidenetetralones misc Cyclic chalcone analogues misc Cell cycle arrest misc Apoptosis misc Colorectal cancer cells
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title	Benzylidenetetralones, cyclic chalcone analogues, induce cell cycle arrest and apoptosis in HCT116 colorectal cancer cells
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title_full	Benzylidenetetralones, cyclic chalcone analogues, induce cell cycle arrest and apoptosis in HCT116 colorectal cancer cells
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author_browse	Drutovic, David Chripkova, Martina Pilatova, Martina Kruzliak, Peter Perjesi, Pal Sarissky, Marek Lupi, Monica Damia, Giovanna Broggini, Massimo Mojzis, Jan
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doi_str_mv	10.1007/s13277-014-2289-y
title_sort	benzylidenetetralones, cyclic chalcone analogues, induce cell cycle arrest and apoptosis in hct116 colorectal cancer cells
title_auth	Benzylidenetetralones, cyclic chalcone analogues, induce cell cycle arrest and apoptosis in HCT116 colorectal cancer cells
abstract	Abstract Colorectal cancer is the third most common cancer in the world, with 1.2 million new cancer cases annually. Chalcones are secondary metabolite precursors of flavonoids that exhibit diverse biological activities, including antioxidant and antitumor activities. The aim of this study was to investigate the antiproliferative effect of new synthetic chalcone derivatives on HCT116 cells. (E)-2-(2′,4′-dimethoxybenzylidene)-1-tetralone (Q705) was found to be the most active ($ IC_{50} $ = 3.44 ± 0.25 μM). Based on these results, this compound was chosen for further analysis of its biochemical and molecular mechanisms. Our results showed that Q705 inhibited the growth and clonogenicity of HCT116 cells. The results of a flow cytometric analyses suggested that this compound caused a significant cell cycle arrest in G2/M phase and increased the proportion of cells in the subG0/G1 phase, marker of apoptosis. Q705-induced apoptosis was confirmed by TdT-mediated dUTP nick end labelling (TUNEL) assay. Treatment of HCT116 cells with this chalcone significantly increased the caspase-3,-7 activity and resulted in cleavage of poly-ADP-ribose polymerase (PARP). Changes in the nuclear morphology such as chromatin condensation were also observed. These effects were associated with a decreased expression of bcl-$ x_{L} $ and increased overall ratio of bax/bcl-$ x_{L} $ mRNA levels. Immunofluorescence and qRT-PCR analysis revealed that Q705 induced H2AX histone modifications characteristic of DNA damage, disruption of microtubule organization and downregulation of tubulins. In summary, these results suggest that the cyclic chalcone analogue Q705 has potential as a new compound for colorectal cancer therapy. © International Society of Oncology and BioMarkers (ISOBM) 2014
abstractGer	Abstract Colorectal cancer is the third most common cancer in the world, with 1.2 million new cancer cases annually. Chalcones are secondary metabolite precursors of flavonoids that exhibit diverse biological activities, including antioxidant and antitumor activities. The aim of this study was to investigate the antiproliferative effect of new synthetic chalcone derivatives on HCT116 cells. (E)-2-(2′,4′-dimethoxybenzylidene)-1-tetralone (Q705) was found to be the most active ($ IC_{50} $ = 3.44 ± 0.25 μM). Based on these results, this compound was chosen for further analysis of its biochemical and molecular mechanisms. Our results showed that Q705 inhibited the growth and clonogenicity of HCT116 cells. The results of a flow cytometric analyses suggested that this compound caused a significant cell cycle arrest in G2/M phase and increased the proportion of cells in the subG0/G1 phase, marker of apoptosis. Q705-induced apoptosis was confirmed by TdT-mediated dUTP nick end labelling (TUNEL) assay. Treatment of HCT116 cells with this chalcone significantly increased the caspase-3,-7 activity and resulted in cleavage of poly-ADP-ribose polymerase (PARP). Changes in the nuclear morphology such as chromatin condensation were also observed. These effects were associated with a decreased expression of bcl-$ x_{L} $ and increased overall ratio of bax/bcl-$ x_{L} $ mRNA levels. Immunofluorescence and qRT-PCR analysis revealed that Q705 induced H2AX histone modifications characteristic of DNA damage, disruption of microtubule organization and downregulation of tubulins. In summary, these results suggest that the cyclic chalcone analogue Q705 has potential as a new compound for colorectal cancer therapy. © International Society of Oncology and BioMarkers (ISOBM) 2014
abstract_unstemmed	Abstract Colorectal cancer is the third most common cancer in the world, with 1.2 million new cancer cases annually. Chalcones are secondary metabolite precursors of flavonoids that exhibit diverse biological activities, including antioxidant and antitumor activities. The aim of this study was to investigate the antiproliferative effect of new synthetic chalcone derivatives on HCT116 cells. (E)-2-(2′,4′-dimethoxybenzylidene)-1-tetralone (Q705) was found to be the most active ($ IC_{50} $ = 3.44 ± 0.25 μM). Based on these results, this compound was chosen for further analysis of its biochemical and molecular mechanisms. Our results showed that Q705 inhibited the growth and clonogenicity of HCT116 cells. The results of a flow cytometric analyses suggested that this compound caused a significant cell cycle arrest in G2/M phase and increased the proportion of cells in the subG0/G1 phase, marker of apoptosis. Q705-induced apoptosis was confirmed by TdT-mediated dUTP nick end labelling (TUNEL) assay. Treatment of HCT116 cells with this chalcone significantly increased the caspase-3,-7 activity and resulted in cleavage of poly-ADP-ribose polymerase (PARP). Changes in the nuclear morphology such as chromatin condensation were also observed. These effects were associated with a decreased expression of bcl-$ x_{L} $ and increased overall ratio of bax/bcl-$ x_{L} $ mRNA levels. Immunofluorescence and qRT-PCR analysis revealed that Q705 induced H2AX histone modifications characteristic of DNA damage, disruption of microtubule organization and downregulation of tubulins. In summary, these results suggest that the cyclic chalcone analogue Q705 has potential as a new compound for colorectal cancer therapy. © International Society of Oncology and BioMarkers (ISOBM) 2014
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title_short	Benzylidenetetralones, cyclic chalcone analogues, induce cell cycle arrest and apoptosis in HCT116 colorectal cancer cells
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Chalcones are secondary metabolite precursors of flavonoids that exhibit diverse biological activities, including antioxidant and antitumor activities. The aim of this study was to investigate the antiproliferative effect of new synthetic chalcone derivatives on HCT116 cells. (E)-2-(2′,4′-dimethoxybenzylidene)-1-tetralone (Q705) was found to be the most active ($ IC_{50} $ = 3.44 ± 0.25 μM). Based on these results, this compound was chosen for further analysis of its biochemical and molecular mechanisms. Our results showed that Q705 inhibited the growth and clonogenicity of HCT116 cells. The results of a flow cytometric analyses suggested that this compound caused a significant cell cycle arrest in G2/M phase and increased the proportion of cells in the subG0/G1 phase, marker of apoptosis. Q705-induced apoptosis was confirmed by TdT-mediated dUTP nick end labelling (TUNEL) assay. Treatment of HCT116 cells with this chalcone significantly increased the caspase-3,-7 activity and resulted in cleavage of poly-ADP-ribose polymerase (PARP). Changes in the nuclear morphology such as chromatin condensation were also observed. These effects were associated with a decreased expression of bcl-$ x_{L} $ and increased overall ratio of bax/bcl-$ x_{L} $ mRNA levels. Immunofluorescence and qRT-PCR analysis revealed that Q705 induced H2AX histone modifications characteristic of DNA damage, disruption of microtubule organization and downregulation of tubulins. 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Benzylidenetetralones, cyclic chalcone analogues, induce cell cycle arrest and apoptosis in HCT116 colorectal cancer cells

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