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Lef-1 Isoforms Regulate Different Target Genes and Reduce Cellular Adhesion by Sarah Jesse; Alexander Koenig; Volker Ellenrieder; Andre Menke is a Medicine article available to read on EtoBox.

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## Abstract The lymphoid enhancer factor 1 (Lef‐1) belongs to the nuclear transducers of canonical Wnt‐signalling in embryogenesis and cancer. Lef‐1 acts, in cooperation with β‐catenin, as a context‐dependent transcriptional activator or repressor, thereby influencing multiple cellular functions such as proliferation, differentiation and migration. Here we report that an increased Lef‐1 expression in human pancreatic cancer correlates with advanced tumour stages. In pancreatic tumours, two different transcripts of Lef‐1 have been detected in various stages, as demonstrated by RT‐PCR analysis. One transcript was identified as the full length Lef‐1 (Lef‐1 FL), whereas the second, shorter transcript lacked exon VI (Lef‐1 Δexon VI) compared to the published sequence. Comparative analysis of these two Lef‐1 variants revealed that they exhibit different cellular effects after transient expression in pancreatic carcinoma cells. Forced expression of Lef‐1 Δexon VI inhibited E‐cadherin expression in a β‐catenin‐independent way. Increased amounts of Lef‐1 Δexon VI resulted in reduced cellular aggregation and increased cell migration. Expression of Lef‐1 FL, but not the newly identified Lef‐1

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Author
Sarah Jesse; Alexander Koenig; Volker Ellenrieder; Andre Menke
Publisher
John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley; Research Square; Test accounts (ISSN 0020-7136)
Published
2009
Language
EN
Field
Medicine (Health Sciences)