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Merck

KITENIN promotes glioma invasiveness and progression, associated with the induction of EMT and stemness markers.

Oncotarget (2015-01-22)
Kyung-Hwa Lee, Eun-Jung Ahn, Se-Jeong Oh, Ok Kim, Young-Eun Joo, Jeong-A Bae, Somy Yoon, Hyang-Hwa Ryu, Shin Jung, Kyung-Keun Kim, Jae-Hyuk Lee, Kyung-Sub Moon
RESUMEN

KITENIN (KAI1 COOH-terminal interacting tetraspanin) promotes tumor invasion and metastasis in various cancers. This study assessed the association between KITENIN expression and advanced glioma grade in patients. In vitro assays revealed that KITENIN knockdown inhibited the invasion and migration of glioma cells, whereas KITENIN overexpression promoted their invasion and migration. In orthotopic mouse tumor models, mice transplanted with KITENIN-transfected glioma cells had significantly shorter survival than mice transplanted with mock-transfected cells. Patients with low KITENIN expression showed a significantly longer progression-free survival than patients with high KITENIN expression. KITENIN induced the expression of the epithelial-mesenchymal transition (EMT) markers (N-cadherin, ZEB1, ZEB2, SNAIL and SLUG) as well as the glioma stemness markers (CD133, ALDH1 and EPH-B1). Taken together, these findings showed that high levels of KITENIN increased glioma invasiveness and progression, associated with the up-regulation of EMT and stemness markers.

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Sigma-Aldrich
Aphidicolin from Nigrospora sphaerica, ≥98% (HPLC), powder
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Anti-VANGL1 antibody produced in rabbit, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
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Aphidicolin, analytical standard
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Anti-VANGL1 antibody produced in rabbit, affinity isolated antibody
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