SLC1A5 Silencing Inhibits Esophageal Cancer Growth via Cell Cycle Arrest and Apoptosis

Background/Aims: Solute-linked carrier family A1 member 5 (SLC1A5), which has high affinity to neutral amino acids, is essential for glutamine transport and amino acid metabolism in various cancers. However, the role of SLC1A5 in esophageal cancer has not been reported. Methods: SLC1A5 expression in...
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Autor*in:	Jieping Lin [verfasserIn] Teng Yang [verfasserIn] Zheng Peng [verfasserIn] Haiyan Xiao [verfasserIn] Na Jiang [verfasserIn] Lifang Zhang [verfasserIn] Dickerson CA [verfasserIn] Ping Wu [verfasserIn] Qingjun Pan [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Schlagwörter:	Slc1a5 Esophageal cancer Glutamine MTORC1

Übergeordnetes Werk:	In: Cellular Physiology and Biochemistry - Cell Physiol Biochem Press GmbH & Co KG, 2002, 48(2018), 1, Seite 397-397
Übergeordnetes Werk:	volume:48 ; year:2018 ; number:1 ; pages:397-397

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1159/000491769

Katalog-ID:	DOAJ002979764

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520			\|a Background/Aims: Solute-linked carrier family A1 member 5 (SLC1A5), which has high affinity to neutral amino acids, is essential for glutamine transport and amino acid metabolism in various cancers. However, the role of SLC1A5 in esophageal cancer has not been reported. Methods: SLC1A5 expression in esophageal cancer tissues was detected by immunohistochemistry and western blotting. The effects of SLC1A5 knockdown on the growth, cell cycle, viability, and glutamine metabolism of esophageal cancer cells were investigated with flow cytometry and western blotting. Furthermore, the consequences of SLC1A5 knockdown on tumor growth and survival were also evaluated in vivo using mice carrying esophageal cancer xenografts. Results: SLC1A5 was expressed in 86.5% (32/37) of the cancer tissues from esophageal cancer patients. Moreover, SLC1A5 expression in the cancerous tissues was significantly higher than that in the paired adjacent normal tissues. SLC1A5 knockdown with siRNA (PZ siRNA) in TE-1 cells in vitro significantly decreased cell growth and reduced both leucine and glutamine transport, leading to inhibition of mTORC1 signaling. Additionally, siRNA-mediated SLC1A5 knockdown resulted in cell cycle arrest and apoptosis of TE-1 cells. The survival rate of athymic (nu/nu) male nude mice carrying tumors formed from TE-1 cells transfected with SLC1A5 siRNA (PZ siRNA) was also significantly improved compared with mice carrying tumors formed from TE-1 cells transfected with control siRNA. Tumor size/weight was also significantly lower for the former mice group of mice. Conclusion: Our data indicate that SLC1A5 plays an important role in esophageal cancer both in vivo and in vitro. The inhibition of esophageal cancer growth by targeting SLC1A5 could, therefore, be used as a preoperative therapy for esophageal cancer.
650		4	\|a Slc1a5
650		4	\|a Esophageal cancer
650		4	\|a Glutamine
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700	0		\|a Teng Yang \|e verfasserin \|4 aut
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700	0		\|a Qingjun Pan \|e verfasserin \|4 aut
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allfields	10.1159/000491769 doi (DE-627)DOAJ002979764 (DE-599)DOAJ98f01bc283f54667b45e5ac2ba7bdd13 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Jieping Lin verfasserin aut SLC1A5 Silencing Inhibits Esophageal Cancer Growth via Cell Cycle Arrest and Apoptosis 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background/Aims: Solute-linked carrier family A1 member 5 (SLC1A5), which has high affinity to neutral amino acids, is essential for glutamine transport and amino acid metabolism in various cancers. However, the role of SLC1A5 in esophageal cancer has not been reported. Methods: SLC1A5 expression in esophageal cancer tissues was detected by immunohistochemistry and western blotting. The effects of SLC1A5 knockdown on the growth, cell cycle, viability, and glutamine metabolism of esophageal cancer cells were investigated with flow cytometry and western blotting. Furthermore, the consequences of SLC1A5 knockdown on tumor growth and survival were also evaluated in vivo using mice carrying esophageal cancer xenografts. Results: SLC1A5 was expressed in 86.5% (32/37) of the cancer tissues from esophageal cancer patients. Moreover, SLC1A5 expression in the cancerous tissues was significantly higher than that in the paired adjacent normal tissues. SLC1A5 knockdown with siRNA (PZ siRNA) in TE-1 cells in vitro significantly decreased cell growth and reduced both leucine and glutamine transport, leading to inhibition of mTORC1 signaling. Additionally, siRNA-mediated SLC1A5 knockdown resulted in cell cycle arrest and apoptosis of TE-1 cells. The survival rate of athymic (nu/nu) male nude mice carrying tumors formed from TE-1 cells transfected with SLC1A5 siRNA (PZ siRNA) was also significantly improved compared with mice carrying tumors formed from TE-1 cells transfected with control siRNA. Tumor size/weight was also significantly lower for the former mice group of mice. Conclusion: Our data indicate that SLC1A5 plays an important role in esophageal cancer both in vivo and in vitro. The inhibition of esophageal cancer growth by targeting SLC1A5 could, therefore, be used as a preoperative therapy for esophageal cancer. Slc1a5 Esophageal cancer Glutamine MTORC1 Physiology Biochemistry Teng Yang verfasserin aut Zheng Peng verfasserin aut Haiyan Xiao verfasserin aut Na Jiang verfasserin aut Lifang Zhang verfasserin aut Dickerson CA verfasserin aut Ping Wu verfasserin aut Qingjun Pan verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 48(2018), 1, Seite 397-397 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:48 year:2018 number:1 pages:397-397 https://doi.org/10.1159/000491769 kostenfrei https://doaj.org/article/98f01bc283f54667b45e5ac2ba7bdd13 kostenfrei https://www.karger.com/Article/FullText/491769 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 48 2018 1 397-397
spelling	10.1159/000491769 doi (DE-627)DOAJ002979764 (DE-599)DOAJ98f01bc283f54667b45e5ac2ba7bdd13 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Jieping Lin verfasserin aut SLC1A5 Silencing Inhibits Esophageal Cancer Growth via Cell Cycle Arrest and Apoptosis 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background/Aims: Solute-linked carrier family A1 member 5 (SLC1A5), which has high affinity to neutral amino acids, is essential for glutamine transport and amino acid metabolism in various cancers. However, the role of SLC1A5 in esophageal cancer has not been reported. Methods: SLC1A5 expression in esophageal cancer tissues was detected by immunohistochemistry and western blotting. The effects of SLC1A5 knockdown on the growth, cell cycle, viability, and glutamine metabolism of esophageal cancer cells were investigated with flow cytometry and western blotting. Furthermore, the consequences of SLC1A5 knockdown on tumor growth and survival were also evaluated in vivo using mice carrying esophageal cancer xenografts. Results: SLC1A5 was expressed in 86.5% (32/37) of the cancer tissues from esophageal cancer patients. Moreover, SLC1A5 expression in the cancerous tissues was significantly higher than that in the paired adjacent normal tissues. SLC1A5 knockdown with siRNA (PZ siRNA) in TE-1 cells in vitro significantly decreased cell growth and reduced both leucine and glutamine transport, leading to inhibition of mTORC1 signaling. Additionally, siRNA-mediated SLC1A5 knockdown resulted in cell cycle arrest and apoptosis of TE-1 cells. The survival rate of athymic (nu/nu) male nude mice carrying tumors formed from TE-1 cells transfected with SLC1A5 siRNA (PZ siRNA) was also significantly improved compared with mice carrying tumors formed from TE-1 cells transfected with control siRNA. Tumor size/weight was also significantly lower for the former mice group of mice. Conclusion: Our data indicate that SLC1A5 plays an important role in esophageal cancer both in vivo and in vitro. The inhibition of esophageal cancer growth by targeting SLC1A5 could, therefore, be used as a preoperative therapy for esophageal cancer. Slc1a5 Esophageal cancer Glutamine MTORC1 Physiology Biochemistry Teng Yang verfasserin aut Zheng Peng verfasserin aut Haiyan Xiao verfasserin aut Na Jiang verfasserin aut Lifang Zhang verfasserin aut Dickerson CA verfasserin aut Ping Wu verfasserin aut Qingjun Pan verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 48(2018), 1, Seite 397-397 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:48 year:2018 number:1 pages:397-397 https://doi.org/10.1159/000491769 kostenfrei https://doaj.org/article/98f01bc283f54667b45e5ac2ba7bdd13 kostenfrei https://www.karger.com/Article/FullText/491769 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 48 2018 1 397-397
allfields_unstemmed	10.1159/000491769 doi (DE-627)DOAJ002979764 (DE-599)DOAJ98f01bc283f54667b45e5ac2ba7bdd13 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Jieping Lin verfasserin aut SLC1A5 Silencing Inhibits Esophageal Cancer Growth via Cell Cycle Arrest and Apoptosis 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background/Aims: Solute-linked carrier family A1 member 5 (SLC1A5), which has high affinity to neutral amino acids, is essential for glutamine transport and amino acid metabolism in various cancers. However, the role of SLC1A5 in esophageal cancer has not been reported. Methods: SLC1A5 expression in esophageal cancer tissues was detected by immunohistochemistry and western blotting. The effects of SLC1A5 knockdown on the growth, cell cycle, viability, and glutamine metabolism of esophageal cancer cells were investigated with flow cytometry and western blotting. Furthermore, the consequences of SLC1A5 knockdown on tumor growth and survival were also evaluated in vivo using mice carrying esophageal cancer xenografts. Results: SLC1A5 was expressed in 86.5% (32/37) of the cancer tissues from esophageal cancer patients. Moreover, SLC1A5 expression in the cancerous tissues was significantly higher than that in the paired adjacent normal tissues. SLC1A5 knockdown with siRNA (PZ siRNA) in TE-1 cells in vitro significantly decreased cell growth and reduced both leucine and glutamine transport, leading to inhibition of mTORC1 signaling. Additionally, siRNA-mediated SLC1A5 knockdown resulted in cell cycle arrest and apoptosis of TE-1 cells. The survival rate of athymic (nu/nu) male nude mice carrying tumors formed from TE-1 cells transfected with SLC1A5 siRNA (PZ siRNA) was also significantly improved compared with mice carrying tumors formed from TE-1 cells transfected with control siRNA. Tumor size/weight was also significantly lower for the former mice group of mice. Conclusion: Our data indicate that SLC1A5 plays an important role in esophageal cancer both in vivo and in vitro. The inhibition of esophageal cancer growth by targeting SLC1A5 could, therefore, be used as a preoperative therapy for esophageal cancer. Slc1a5 Esophageal cancer Glutamine MTORC1 Physiology Biochemistry Teng Yang verfasserin aut Zheng Peng verfasserin aut Haiyan Xiao verfasserin aut Na Jiang verfasserin aut Lifang Zhang verfasserin aut Dickerson CA verfasserin aut Ping Wu verfasserin aut Qingjun Pan verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 48(2018), 1, Seite 397-397 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:48 year:2018 number:1 pages:397-397 https://doi.org/10.1159/000491769 kostenfrei https://doaj.org/article/98f01bc283f54667b45e5ac2ba7bdd13 kostenfrei https://www.karger.com/Article/FullText/491769 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 48 2018 1 397-397
allfieldsGer	10.1159/000491769 doi (DE-627)DOAJ002979764 (DE-599)DOAJ98f01bc283f54667b45e5ac2ba7bdd13 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Jieping Lin verfasserin aut SLC1A5 Silencing Inhibits Esophageal Cancer Growth via Cell Cycle Arrest and Apoptosis 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background/Aims: Solute-linked carrier family A1 member 5 (SLC1A5), which has high affinity to neutral amino acids, is essential for glutamine transport and amino acid metabolism in various cancers. However, the role of SLC1A5 in esophageal cancer has not been reported. Methods: SLC1A5 expression in esophageal cancer tissues was detected by immunohistochemistry and western blotting. The effects of SLC1A5 knockdown on the growth, cell cycle, viability, and glutamine metabolism of esophageal cancer cells were investigated with flow cytometry and western blotting. Furthermore, the consequences of SLC1A5 knockdown on tumor growth and survival were also evaluated in vivo using mice carrying esophageal cancer xenografts. Results: SLC1A5 was expressed in 86.5% (32/37) of the cancer tissues from esophageal cancer patients. Moreover, SLC1A5 expression in the cancerous tissues was significantly higher than that in the paired adjacent normal tissues. SLC1A5 knockdown with siRNA (PZ siRNA) in TE-1 cells in vitro significantly decreased cell growth and reduced both leucine and glutamine transport, leading to inhibition of mTORC1 signaling. Additionally, siRNA-mediated SLC1A5 knockdown resulted in cell cycle arrest and apoptosis of TE-1 cells. The survival rate of athymic (nu/nu) male nude mice carrying tumors formed from TE-1 cells transfected with SLC1A5 siRNA (PZ siRNA) was also significantly improved compared with mice carrying tumors formed from TE-1 cells transfected with control siRNA. Tumor size/weight was also significantly lower for the former mice group of mice. Conclusion: Our data indicate that SLC1A5 plays an important role in esophageal cancer both in vivo and in vitro. The inhibition of esophageal cancer growth by targeting SLC1A5 could, therefore, be used as a preoperative therapy for esophageal cancer. Slc1a5 Esophageal cancer Glutamine MTORC1 Physiology Biochemistry Teng Yang verfasserin aut Zheng Peng verfasserin aut Haiyan Xiao verfasserin aut Na Jiang verfasserin aut Lifang Zhang verfasserin aut Dickerson CA verfasserin aut Ping Wu verfasserin aut Qingjun Pan verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 48(2018), 1, Seite 397-397 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:48 year:2018 number:1 pages:397-397 https://doi.org/10.1159/000491769 kostenfrei https://doaj.org/article/98f01bc283f54667b45e5ac2ba7bdd13 kostenfrei https://www.karger.com/Article/FullText/491769 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 48 2018 1 397-397
allfieldsSound	10.1159/000491769 doi (DE-627)DOAJ002979764 (DE-599)DOAJ98f01bc283f54667b45e5ac2ba7bdd13 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Jieping Lin verfasserin aut SLC1A5 Silencing Inhibits Esophageal Cancer Growth via Cell Cycle Arrest and Apoptosis 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background/Aims: Solute-linked carrier family A1 member 5 (SLC1A5), which has high affinity to neutral amino acids, is essential for glutamine transport and amino acid metabolism in various cancers. However, the role of SLC1A5 in esophageal cancer has not been reported. Methods: SLC1A5 expression in esophageal cancer tissues was detected by immunohistochemistry and western blotting. The effects of SLC1A5 knockdown on the growth, cell cycle, viability, and glutamine metabolism of esophageal cancer cells were investigated with flow cytometry and western blotting. Furthermore, the consequences of SLC1A5 knockdown on tumor growth and survival were also evaluated in vivo using mice carrying esophageal cancer xenografts. Results: SLC1A5 was expressed in 86.5% (32/37) of the cancer tissues from esophageal cancer patients. Moreover, SLC1A5 expression in the cancerous tissues was significantly higher than that in the paired adjacent normal tissues. SLC1A5 knockdown with siRNA (PZ siRNA) in TE-1 cells in vitro significantly decreased cell growth and reduced both leucine and glutamine transport, leading to inhibition of mTORC1 signaling. Additionally, siRNA-mediated SLC1A5 knockdown resulted in cell cycle arrest and apoptosis of TE-1 cells. The survival rate of athymic (nu/nu) male nude mice carrying tumors formed from TE-1 cells transfected with SLC1A5 siRNA (PZ siRNA) was also significantly improved compared with mice carrying tumors formed from TE-1 cells transfected with control siRNA. Tumor size/weight was also significantly lower for the former mice group of mice. Conclusion: Our data indicate that SLC1A5 plays an important role in esophageal cancer both in vivo and in vitro. The inhibition of esophageal cancer growth by targeting SLC1A5 could, therefore, be used as a preoperative therapy for esophageal cancer. Slc1a5 Esophageal cancer Glutamine MTORC1 Physiology Biochemistry Teng Yang verfasserin aut Zheng Peng verfasserin aut Haiyan Xiao verfasserin aut Na Jiang verfasserin aut Lifang Zhang verfasserin aut Dickerson CA verfasserin aut Ping Wu verfasserin aut Qingjun Pan verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 48(2018), 1, Seite 397-397 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:48 year:2018 number:1 pages:397-397 https://doi.org/10.1159/000491769 kostenfrei https://doaj.org/article/98f01bc283f54667b45e5ac2ba7bdd13 kostenfrei https://www.karger.com/Article/FullText/491769 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 48 2018 1 397-397
language	English
source	In Cellular Physiology and Biochemistry 48(2018), 1, Seite 397-397 volume:48 year:2018 number:1 pages:397-397
sourceStr	In Cellular Physiology and Biochemistry 48(2018), 1, Seite 397-397 volume:48 year:2018 number:1 pages:397-397
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Slc1a5 Esophageal cancer Glutamine MTORC1 Physiology Biochemistry
isfreeaccess_bool	true
container_title	Cellular Physiology and Biochemistry
authorswithroles_txt_mv	Jieping Lin @@aut@@ Teng Yang @@aut@@ Zheng Peng @@aut@@ Haiyan Xiao @@aut@@ Na Jiang @@aut@@ Lifang Zhang @@aut@@ Dickerson CA @@aut@@ Ping Wu @@aut@@ Qingjun Pan @@aut@@
publishDateDaySort_date	2018-01-01T00:00:00Z
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author	Jieping Lin
spellingShingle	Jieping Lin misc QP1-981 misc QD415-436 misc Slc1a5 misc Esophageal cancer misc Glutamine misc MTORC1 misc Physiology misc Biochemistry SLC1A5 Silencing Inhibits Esophageal Cancer Growth via Cell Cycle Arrest and Apoptosis
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issn	14219778
topic_title	QP1-981 QD415-436 SLC1A5 Silencing Inhibits Esophageal Cancer Growth via Cell Cycle Arrest and Apoptosis Slc1a5 Esophageal cancer Glutamine MTORC1
topic	misc QP1-981 misc QD415-436 misc Slc1a5 misc Esophageal cancer misc Glutamine misc MTORC1 misc Physiology misc Biochemistry
topic_unstemmed	misc QP1-981 misc QD415-436 misc Slc1a5 misc Esophageal cancer misc Glutamine misc MTORC1 misc Physiology misc Biochemistry
topic_browse	misc QP1-981 misc QD415-436 misc Slc1a5 misc Esophageal cancer misc Glutamine misc MTORC1 misc Physiology misc Biochemistry
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title	SLC1A5 Silencing Inhibits Esophageal Cancer Growth via Cell Cycle Arrest and Apoptosis
ctrlnum	(DE-627)DOAJ002979764 (DE-599)DOAJ98f01bc283f54667b45e5ac2ba7bdd13
title_full	SLC1A5 Silencing Inhibits Esophageal Cancer Growth via Cell Cycle Arrest and Apoptosis
author_sort	Jieping Lin
journal	Cellular Physiology and Biochemistry
journalStr	Cellular Physiology and Biochemistry
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author_browse	Jieping Lin Teng Yang Zheng Peng Haiyan Xiao Na Jiang Lifang Zhang Dickerson CA Ping Wu Qingjun Pan
container_volume	48
class	QP1-981 QD415-436
format_se	Elektronische Aufsätze
author-letter	Jieping Lin
doi_str_mv	10.1159/000491769
author2-role	verfasserin
title_sort	slc1a5 silencing inhibits esophageal cancer growth via cell cycle arrest and apoptosis
callnumber	QP1-981
title_auth	SLC1A5 Silencing Inhibits Esophageal Cancer Growth via Cell Cycle Arrest and Apoptosis
abstract	Background/Aims: Solute-linked carrier family A1 member 5 (SLC1A5), which has high affinity to neutral amino acids, is essential for glutamine transport and amino acid metabolism in various cancers. However, the role of SLC1A5 in esophageal cancer has not been reported. Methods: SLC1A5 expression in esophageal cancer tissues was detected by immunohistochemistry and western blotting. The effects of SLC1A5 knockdown on the growth, cell cycle, viability, and glutamine metabolism of esophageal cancer cells were investigated with flow cytometry and western blotting. Furthermore, the consequences of SLC1A5 knockdown on tumor growth and survival were also evaluated in vivo using mice carrying esophageal cancer xenografts. Results: SLC1A5 was expressed in 86.5% (32/37) of the cancer tissues from esophageal cancer patients. Moreover, SLC1A5 expression in the cancerous tissues was significantly higher than that in the paired adjacent normal tissues. SLC1A5 knockdown with siRNA (PZ siRNA) in TE-1 cells in vitro significantly decreased cell growth and reduced both leucine and glutamine transport, leading to inhibition of mTORC1 signaling. Additionally, siRNA-mediated SLC1A5 knockdown resulted in cell cycle arrest and apoptosis of TE-1 cells. The survival rate of athymic (nu/nu) male nude mice carrying tumors formed from TE-1 cells transfected with SLC1A5 siRNA (PZ siRNA) was also significantly improved compared with mice carrying tumors formed from TE-1 cells transfected with control siRNA. Tumor size/weight was also significantly lower for the former mice group of mice. Conclusion: Our data indicate that SLC1A5 plays an important role in esophageal cancer both in vivo and in vitro. The inhibition of esophageal cancer growth by targeting SLC1A5 could, therefore, be used as a preoperative therapy for esophageal cancer.
abstractGer	Background/Aims: Solute-linked carrier family A1 member 5 (SLC1A5), which has high affinity to neutral amino acids, is essential for glutamine transport and amino acid metabolism in various cancers. However, the role of SLC1A5 in esophageal cancer has not been reported. Methods: SLC1A5 expression in esophageal cancer tissues was detected by immunohistochemistry and western blotting. The effects of SLC1A5 knockdown on the growth, cell cycle, viability, and glutamine metabolism of esophageal cancer cells were investigated with flow cytometry and western blotting. Furthermore, the consequences of SLC1A5 knockdown on tumor growth and survival were also evaluated in vivo using mice carrying esophageal cancer xenografts. Results: SLC1A5 was expressed in 86.5% (32/37) of the cancer tissues from esophageal cancer patients. Moreover, SLC1A5 expression in the cancerous tissues was significantly higher than that in the paired adjacent normal tissues. SLC1A5 knockdown with siRNA (PZ siRNA) in TE-1 cells in vitro significantly decreased cell growth and reduced both leucine and glutamine transport, leading to inhibition of mTORC1 signaling. Additionally, siRNA-mediated SLC1A5 knockdown resulted in cell cycle arrest and apoptosis of TE-1 cells. The survival rate of athymic (nu/nu) male nude mice carrying tumors formed from TE-1 cells transfected with SLC1A5 siRNA (PZ siRNA) was also significantly improved compared with mice carrying tumors formed from TE-1 cells transfected with control siRNA. Tumor size/weight was also significantly lower for the former mice group of mice. Conclusion: Our data indicate that SLC1A5 plays an important role in esophageal cancer both in vivo and in vitro. The inhibition of esophageal cancer growth by targeting SLC1A5 could, therefore, be used as a preoperative therapy for esophageal cancer.
abstract_unstemmed	Background/Aims: Solute-linked carrier family A1 member 5 (SLC1A5), which has high affinity to neutral amino acids, is essential for glutamine transport and amino acid metabolism in various cancers. However, the role of SLC1A5 in esophageal cancer has not been reported. Methods: SLC1A5 expression in esophageal cancer tissues was detected by immunohistochemistry and western blotting. The effects of SLC1A5 knockdown on the growth, cell cycle, viability, and glutamine metabolism of esophageal cancer cells were investigated with flow cytometry and western blotting. Furthermore, the consequences of SLC1A5 knockdown on tumor growth and survival were also evaluated in vivo using mice carrying esophageal cancer xenografts. Results: SLC1A5 was expressed in 86.5% (32/37) of the cancer tissues from esophageal cancer patients. Moreover, SLC1A5 expression in the cancerous tissues was significantly higher than that in the paired adjacent normal tissues. SLC1A5 knockdown with siRNA (PZ siRNA) in TE-1 cells in vitro significantly decreased cell growth and reduced both leucine and glutamine transport, leading to inhibition of mTORC1 signaling. Additionally, siRNA-mediated SLC1A5 knockdown resulted in cell cycle arrest and apoptosis of TE-1 cells. The survival rate of athymic (nu/nu) male nude mice carrying tumors formed from TE-1 cells transfected with SLC1A5 siRNA (PZ siRNA) was also significantly improved compared with mice carrying tumors formed from TE-1 cells transfected with control siRNA. Tumor size/weight was also significantly lower for the former mice group of mice. Conclusion: Our data indicate that SLC1A5 plays an important role in esophageal cancer both in vivo and in vitro. The inhibition of esophageal cancer growth by targeting SLC1A5 could, therefore, be used as a preoperative therapy for esophageal cancer.
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container_issue	1
title_short	SLC1A5 Silencing Inhibits Esophageal Cancer Growth via Cell Cycle Arrest and Apoptosis
url	https://doi.org/10.1159/000491769 https://doaj.org/article/98f01bc283f54667b45e5ac2ba7bdd13 https://www.karger.com/Article/FullText/491769 https://doaj.org/toc/1015-8987 https://doaj.org/toc/1421-9778
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author2	Teng Yang Zheng Peng Haiyan Xiao Na Jiang Lifang Zhang Dickerson CA Ping Wu Qingjun Pan
author2Str	Teng Yang Zheng Peng Haiyan Xiao Na Jiang Lifang Zhang Dickerson CA Ping Wu Qingjun Pan
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up_date	2024-07-03T15:14:40.293Z
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