Combination treatment with perifosine and MEK-162 demonstrates synergism against lung cancer cells in vitro and in vivo

Abstract Lung cancer is a global health problem. The search for new therapeutic approaches for the treatment of lung cancer is important. Here, we reported that the AKT inhibitor perifosine and the MEK\ERK inhibitor MEK-162 synergistically induced lung cancer cell (A549 and H460 lines) growth inhibi...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Zhang, Jianli [verfasserIn] Hong, Yue Shen, Jie

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2015

Schlagwörter:	Lung cancer Perifosine MEK-162 PI3K-AKT-mTOR MEK-ERK Synergism

Anmerkung:	© International Society of Oncology and BioMarkers (ISOBM) 2015

Übergeordnetes Werk:	Enthalten in: Tumor biology - Amsterdam : IOS Press, 1987, 36(2015), 7 vom: 20. Feb., Seite 5699-5706
Übergeordnetes Werk:	volume:36 ; year:2015 ; number:7 ; day:20 ; month:02 ; pages:5699-5706

Links:	Volltext

DOI / URN:	10.1007/s13277-015-3244-2

Katalog-ID:	SPR03115946X

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allfields	10.1007/s13277-015-3244-2 doi (DE-627)SPR03115946X (SPR)s13277-015-3244-2-e DE-627 ger DE-627 rakwb eng Zhang, Jianli verfasserin aut Combination treatment with perifosine and MEK-162 demonstrates synergism against lung cancer cells in vitro and in vivo 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2015 Abstract Lung cancer is a global health problem. The search for new therapeutic approaches for the treatment of lung cancer is important. Here, we reported that the AKT inhibitor perifosine and the MEK\ERK inhibitor MEK-162 synergistically induced lung cancer cell (A549 and H460 lines) growth inhibition and apoptosis. The combined efficiency was significantly higher than either agent alone. For the molecular study, perifosine and MEK-162 worked together to concurrently block AKT, mammalian target of rapamycin (mTOR) complex 1 (mTORC1), and MEK-ERK signalings in lung cancer cells, while either agent alone only affected one or two signalings with lower efficiency. In vivo, MEK-162 and perifosine co-administration dramatically inhibited A549 lung cancer xenograft growth, without inducing apparent toxicities. The synergistic activity in vivo was again superior than either agent alone. Thus, perifosine and MEK-162 combination is biologically plausible by acting through effects on different proliferation and survival-related signaling pathways. Our in vitro and in vivo results support the feasibility of investigating the synergism regimen in clinical tests. Lung cancer (dpeaa)DE-He213 Perifosine (dpeaa)DE-He213 MEK-162 (dpeaa)DE-He213 PI3K-AKT-mTOR (dpeaa)DE-He213 MEK-ERK (dpeaa)DE-He213 Synergism (dpeaa)DE-He213 Hong, Yue aut Shen, Jie aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 36(2015), 7 vom: 20. Feb., Seite 5699-5706 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:36 year:2015 number:7 day:20 month:02 pages:5699-5706 https://dx.doi.org/10.1007/s13277-015-3244-2 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_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 36 2015 7 20 02 5699-5706
spelling	10.1007/s13277-015-3244-2 doi (DE-627)SPR03115946X (SPR)s13277-015-3244-2-e DE-627 ger DE-627 rakwb eng Zhang, Jianli verfasserin aut Combination treatment with perifosine and MEK-162 demonstrates synergism against lung cancer cells in vitro and in vivo 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2015 Abstract Lung cancer is a global health problem. The search for new therapeutic approaches for the treatment of lung cancer is important. Here, we reported that the AKT inhibitor perifosine and the MEK\ERK inhibitor MEK-162 synergistically induced lung cancer cell (A549 and H460 lines) growth inhibition and apoptosis. The combined efficiency was significantly higher than either agent alone. For the molecular study, perifosine and MEK-162 worked together to concurrently block AKT, mammalian target of rapamycin (mTOR) complex 1 (mTORC1), and MEK-ERK signalings in lung cancer cells, while either agent alone only affected one or two signalings with lower efficiency. In vivo, MEK-162 and perifosine co-administration dramatically inhibited A549 lung cancer xenograft growth, without inducing apparent toxicities. The synergistic activity in vivo was again superior than either agent alone. Thus, perifosine and MEK-162 combination is biologically plausible by acting through effects on different proliferation and survival-related signaling pathways. Our in vitro and in vivo results support the feasibility of investigating the synergism regimen in clinical tests. Lung cancer (dpeaa)DE-He213 Perifosine (dpeaa)DE-He213 MEK-162 (dpeaa)DE-He213 PI3K-AKT-mTOR (dpeaa)DE-He213 MEK-ERK (dpeaa)DE-He213 Synergism (dpeaa)DE-He213 Hong, Yue aut Shen, Jie aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 36(2015), 7 vom: 20. Feb., Seite 5699-5706 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:36 year:2015 number:7 day:20 month:02 pages:5699-5706 https://dx.doi.org/10.1007/s13277-015-3244-2 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_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 36 2015 7 20 02 5699-5706
allfields_unstemmed	10.1007/s13277-015-3244-2 doi (DE-627)SPR03115946X (SPR)s13277-015-3244-2-e DE-627 ger DE-627 rakwb eng Zhang, Jianli verfasserin aut Combination treatment with perifosine and MEK-162 demonstrates synergism against lung cancer cells in vitro and in vivo 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2015 Abstract Lung cancer is a global health problem. The search for new therapeutic approaches for the treatment of lung cancer is important. Here, we reported that the AKT inhibitor perifosine and the MEK\ERK inhibitor MEK-162 synergistically induced lung cancer cell (A549 and H460 lines) growth inhibition and apoptosis. The combined efficiency was significantly higher than either agent alone. For the molecular study, perifosine and MEK-162 worked together to concurrently block AKT, mammalian target of rapamycin (mTOR) complex 1 (mTORC1), and MEK-ERK signalings in lung cancer cells, while either agent alone only affected one or two signalings with lower efficiency. In vivo, MEK-162 and perifosine co-administration dramatically inhibited A549 lung cancer xenograft growth, without inducing apparent toxicities. The synergistic activity in vivo was again superior than either agent alone. Thus, perifosine and MEK-162 combination is biologically plausible by acting through effects on different proliferation and survival-related signaling pathways. Our in vitro and in vivo results support the feasibility of investigating the synergism regimen in clinical tests. Lung cancer (dpeaa)DE-He213 Perifosine (dpeaa)DE-He213 MEK-162 (dpeaa)DE-He213 PI3K-AKT-mTOR (dpeaa)DE-He213 MEK-ERK (dpeaa)DE-He213 Synergism (dpeaa)DE-He213 Hong, Yue aut Shen, Jie aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 36(2015), 7 vom: 20. Feb., Seite 5699-5706 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:36 year:2015 number:7 day:20 month:02 pages:5699-5706 https://dx.doi.org/10.1007/s13277-015-3244-2 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_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 36 2015 7 20 02 5699-5706
allfieldsGer	10.1007/s13277-015-3244-2 doi (DE-627)SPR03115946X (SPR)s13277-015-3244-2-e DE-627 ger DE-627 rakwb eng Zhang, Jianli verfasserin aut Combination treatment with perifosine and MEK-162 demonstrates synergism against lung cancer cells in vitro and in vivo 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2015 Abstract Lung cancer is a global health problem. The search for new therapeutic approaches for the treatment of lung cancer is important. Here, we reported that the AKT inhibitor perifosine and the MEK\ERK inhibitor MEK-162 synergistically induced lung cancer cell (A549 and H460 lines) growth inhibition and apoptosis. The combined efficiency was significantly higher than either agent alone. For the molecular study, perifosine and MEK-162 worked together to concurrently block AKT, mammalian target of rapamycin (mTOR) complex 1 (mTORC1), and MEK-ERK signalings in lung cancer cells, while either agent alone only affected one or two signalings with lower efficiency. In vivo, MEK-162 and perifosine co-administration dramatically inhibited A549 lung cancer xenograft growth, without inducing apparent toxicities. The synergistic activity in vivo was again superior than either agent alone. Thus, perifosine and MEK-162 combination is biologically plausible by acting through effects on different proliferation and survival-related signaling pathways. Our in vitro and in vivo results support the feasibility of investigating the synergism regimen in clinical tests. Lung cancer (dpeaa)DE-He213 Perifosine (dpeaa)DE-He213 MEK-162 (dpeaa)DE-He213 PI3K-AKT-mTOR (dpeaa)DE-He213 MEK-ERK (dpeaa)DE-He213 Synergism (dpeaa)DE-He213 Hong, Yue aut Shen, Jie aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 36(2015), 7 vom: 20. Feb., Seite 5699-5706 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:36 year:2015 number:7 day:20 month:02 pages:5699-5706 https://dx.doi.org/10.1007/s13277-015-3244-2 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_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 36 2015 7 20 02 5699-5706
allfieldsSound	10.1007/s13277-015-3244-2 doi (DE-627)SPR03115946X (SPR)s13277-015-3244-2-e DE-627 ger DE-627 rakwb eng Zhang, Jianli verfasserin aut Combination treatment with perifosine and MEK-162 demonstrates synergism against lung cancer cells in vitro and in vivo 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2015 Abstract Lung cancer is a global health problem. The search for new therapeutic approaches for the treatment of lung cancer is important. Here, we reported that the AKT inhibitor perifosine and the MEK\ERK inhibitor MEK-162 synergistically induced lung cancer cell (A549 and H460 lines) growth inhibition and apoptosis. The combined efficiency was significantly higher than either agent alone. For the molecular study, perifosine and MEK-162 worked together to concurrently block AKT, mammalian target of rapamycin (mTOR) complex 1 (mTORC1), and MEK-ERK signalings in lung cancer cells, while either agent alone only affected one or two signalings with lower efficiency. In vivo, MEK-162 and perifosine co-administration dramatically inhibited A549 lung cancer xenograft growth, without inducing apparent toxicities. The synergistic activity in vivo was again superior than either agent alone. Thus, perifosine and MEK-162 combination is biologically plausible by acting through effects on different proliferation and survival-related signaling pathways. Our in vitro and in vivo results support the feasibility of investigating the synergism regimen in clinical tests. Lung cancer (dpeaa)DE-He213 Perifosine (dpeaa)DE-He213 MEK-162 (dpeaa)DE-He213 PI3K-AKT-mTOR (dpeaa)DE-He213 MEK-ERK (dpeaa)DE-He213 Synergism (dpeaa)DE-He213 Hong, Yue aut Shen, Jie aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 36(2015), 7 vom: 20. Feb., Seite 5699-5706 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:36 year:2015 number:7 day:20 month:02 pages:5699-5706 https://dx.doi.org/10.1007/s13277-015-3244-2 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_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 36 2015 7 20 02 5699-5706
language	English
source	Enthalten in Tumor biology 36(2015), 7 vom: 20. Feb., Seite 5699-5706 volume:36 year:2015 number:7 day:20 month:02 pages:5699-5706
sourceStr	Enthalten in Tumor biology 36(2015), 7 vom: 20. Feb., Seite 5699-5706 volume:36 year:2015 number:7 day:20 month:02 pages:5699-5706
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Lung cancer Perifosine MEK-162 PI3K-AKT-mTOR MEK-ERK Synergism
isfreeaccess_bool	false
container_title	Tumor biology
authorswithroles_txt_mv	Zhang, Jianli @@aut@@ Hong, Yue @@aut@@ Shen, Jie @@aut@@
publishDateDaySort_date	2015-02-20T00:00:00Z
hierarchy_top_id	300897855
id	SPR03115946X
language_de	englisch
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author	Zhang, Jianli
spellingShingle	Zhang, Jianli misc Lung cancer misc Perifosine misc MEK-162 misc PI3K-AKT-mTOR misc MEK-ERK misc Synergism Combination treatment with perifosine and MEK-162 demonstrates synergism against lung cancer cells in vitro and in vivo
authorStr	Zhang, Jianli
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topic_title	Combination treatment with perifosine and MEK-162 demonstrates synergism against lung cancer cells in vitro and in vivo Lung cancer (dpeaa)DE-He213 Perifosine (dpeaa)DE-He213 MEK-162 (dpeaa)DE-He213 PI3K-AKT-mTOR (dpeaa)DE-He213 MEK-ERK (dpeaa)DE-He213 Synergism (dpeaa)DE-He213
topic	misc Lung cancer misc Perifosine misc MEK-162 misc PI3K-AKT-mTOR misc MEK-ERK misc Synergism
topic_unstemmed	misc Lung cancer misc Perifosine misc MEK-162 misc PI3K-AKT-mTOR misc MEK-ERK misc Synergism
topic_browse	misc Lung cancer misc Perifosine misc MEK-162 misc PI3K-AKT-mTOR misc MEK-ERK misc Synergism
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title	Combination treatment with perifosine and MEK-162 demonstrates synergism against lung cancer cells in vitro and in vivo
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title_full	Combination treatment with perifosine and MEK-162 demonstrates synergism against lung cancer cells in vitro and in vivo
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author_browse	Zhang, Jianli Hong, Yue Shen, Jie
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author-letter	Zhang, Jianli
doi_str_mv	10.1007/s13277-015-3244-2
title_sort	combination treatment with perifosine and mek-162 demonstrates synergism against lung cancer cells in vitro and in vivo
title_auth	Combination treatment with perifosine and MEK-162 demonstrates synergism against lung cancer cells in vitro and in vivo
abstract	Abstract Lung cancer is a global health problem. The search for new therapeutic approaches for the treatment of lung cancer is important. Here, we reported that the AKT inhibitor perifosine and the MEK\ERK inhibitor MEK-162 synergistically induced lung cancer cell (A549 and H460 lines) growth inhibition and apoptosis. The combined efficiency was significantly higher than either agent alone. For the molecular study, perifosine and MEK-162 worked together to concurrently block AKT, mammalian target of rapamycin (mTOR) complex 1 (mTORC1), and MEK-ERK signalings in lung cancer cells, while either agent alone only affected one or two signalings with lower efficiency. In vivo, MEK-162 and perifosine co-administration dramatically inhibited A549 lung cancer xenograft growth, without inducing apparent toxicities. The synergistic activity in vivo was again superior than either agent alone. Thus, perifosine and MEK-162 combination is biologically plausible by acting through effects on different proliferation and survival-related signaling pathways. Our in vitro and in vivo results support the feasibility of investigating the synergism regimen in clinical tests. © International Society of Oncology and BioMarkers (ISOBM) 2015
abstractGer	Abstract Lung cancer is a global health problem. The search for new therapeutic approaches for the treatment of lung cancer is important. Here, we reported that the AKT inhibitor perifosine and the MEK\ERK inhibitor MEK-162 synergistically induced lung cancer cell (A549 and H460 lines) growth inhibition and apoptosis. The combined efficiency was significantly higher than either agent alone. For the molecular study, perifosine and MEK-162 worked together to concurrently block AKT, mammalian target of rapamycin (mTOR) complex 1 (mTORC1), and MEK-ERK signalings in lung cancer cells, while either agent alone only affected one or two signalings with lower efficiency. In vivo, MEK-162 and perifosine co-administration dramatically inhibited A549 lung cancer xenograft growth, without inducing apparent toxicities. The synergistic activity in vivo was again superior than either agent alone. Thus, perifosine and MEK-162 combination is biologically plausible by acting through effects on different proliferation and survival-related signaling pathways. Our in vitro and in vivo results support the feasibility of investigating the synergism regimen in clinical tests. © International Society of Oncology and BioMarkers (ISOBM) 2015
abstract_unstemmed	Abstract Lung cancer is a global health problem. The search for new therapeutic approaches for the treatment of lung cancer is important. Here, we reported that the AKT inhibitor perifosine and the MEK\ERK inhibitor MEK-162 synergistically induced lung cancer cell (A549 and H460 lines) growth inhibition and apoptosis. The combined efficiency was significantly higher than either agent alone. For the molecular study, perifosine and MEK-162 worked together to concurrently block AKT, mammalian target of rapamycin (mTOR) complex 1 (mTORC1), and MEK-ERK signalings in lung cancer cells, while either agent alone only affected one or two signalings with lower efficiency. In vivo, MEK-162 and perifosine co-administration dramatically inhibited A549 lung cancer xenograft growth, without inducing apparent toxicities. The synergistic activity in vivo was again superior than either agent alone. Thus, perifosine and MEK-162 combination is biologically plausible by acting through effects on different proliferation and survival-related signaling pathways. Our in vitro and in vivo results support the feasibility of investigating the synergism regimen in clinical tests. © International Society of Oncology and BioMarkers (ISOBM) 2015
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title_short	Combination treatment with perifosine and MEK-162 demonstrates synergism against lung cancer cells in vitro and in vivo
url	https://dx.doi.org/10.1007/s13277-015-3244-2
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Combination treatment with perifosine and MEK-162 demonstrates synergism against lung cancer cells in vitro and in vivo

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