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Status: Bibliographieeintrag

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Verfasst von:Bruns, Helge [VerfasserIn]   i
 Kazanavičius, Darius [VerfasserIn]   i
 Schultze, Daniel [VerfasserIn]   i
 Saeedi, Mohammed al [VerfasserIn]   i
 Yamanaka, Kenia [VerfasserIn]   i
 Strupas, Kestutis [VerfasserIn]   i
 Schemmer, Peter [VerfasserIn]   i
Titel:Glycine inhibits angiogenesis in colorectal cancer
Titelzusatz:role of endothelial cells
Verf.angabe:Helge Bruns, Darius Kazanavicius, Daniel Schultze, Mohammed Al Saeedi, Kenia Yamanaka, Kestutis Strupas, Peter Schemmer
E-Jahr:2016
Jahr:28 June 2016
Umfang:10 S.
Fussnoten:Gesehen am 20.05.2020
Titel Quelle:Enthalten in: Amino acids
Ort Quelle:Wien [u.a.] : Springer, 1991
Jahr Quelle:2016
Band/Heft Quelle:48(2016), 11, Seite 2549-2558
ISSN Quelle:1438-2199
Abstract:Neo-angiogenesis is important for tumor growth. Glycine is a non-toxic amino acid with suspected anti-angiogenic effects. This study was designed to evaluate anti-angiogenic effects of glycine in colorectal cancer. Glycine was added to cultures of human and rat colorectal cancer cells (CRC), and endothelial cells (HUVEC). Glycine’s direct impact was monitored using MTT assays. Angiogenesis in HUVEC was monitored using 3D sprouting and migration assays. VEGF and CRC-conditioned media were used to stimulate angiogenesis. The glycine receptor (GlyR) was detected using Western blotting and inhibited using strychnine. The WAG-Rij/CC-531 model of metastatic CRC was used to evaluate glycine’s impact in vivo. Tumor growth and vessel density were monitored in rats fed with or without 5 % glycine for 14 days. VEGF and conditioned media significantly increased proliferation, migration, and capillary formation to up to 267 %. Glycine completely neutralized this effect and strychnine completely blunted glycine’s effect. GlyR was detected in HUVEC. Tumor volume, weight, and vessel density decreased by 35 % (p = 0.02), 34 % (p = 0.03), and 55 % (p = 0.04) in glycine-fed animals. Glycine inhibits angiogenic signaling of endothelial cells and tumor growth. Glycine would be a promising additive to standard and targeted cancer therapies.
DOI:doi:10.1007/s00726-016-2278-0
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1007/s00726-016-2278-0
 DOI: https://doi.org/10.1007/s00726-016-2278-0
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:169862106X
Verknüpfungen:→ Zeitschrift

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