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- Title
Loss of PTPN23 Promotes Proliferation and Epithelial-to-Mesenchymal Transition in Human Intestinal Cancer Cells.
- Authors
van der Lely, Lisa; Häfliger, Janine; Montalban-Arques, Ana; Bäbler, Katharina; Schwarzfischer, Marlene; Sabev, Max; Gottier, Claudia; Lang, Silvia; Scharl, Michael; Spalinger, Marianne R.
- Abstract
Background/Objectives: Protein tyrosine phosphatase nonreceptor type 23 (PTPN23) has recently been associated with several human epithelial cancers via regulation of growth factor signaling. Colorectal carcinoma (CRC) is a leading cause for cancer-related death worldwide and is associated with aberrant epidermal (EGF) and vascular endothelial growth factor signaling. Here, we investigated whether PTPN23 might play a role in CRC. Methods: Expression of PTPN23 was analyzed in CRC tissue by immunohistochemistry. PTPN23 was silenced in HT-29 cells to address the role of PTPN23 in EGF signaling, gene expression, and cell migration. Results: PTPN23 silencing in HT-29 and Caco-2 intestinal epithelial cancer cells significantly enhanced activation of pro-oncogenic signaling molecules and genes promoting epithelial-to-mesenchymal transition (EMT) upon EGF treatment, while genes encoding tight junction proteins were significantly reduced. Conclusions: Our data clearly indicate that loss of PTPN23 is associated with increased activation of pro-oncogenic signaling pathways and an enhanced ability of human intestinal cancer cells to undergo EMT. Taken together, these findings show that PTPN23 acts as a tumor suppressor gene in CRC.
- Publication
Inflammatory Intestinal Diseases, 2019, Vol 4, Issue 4, p161
- ISSN
2296-9403
- Publication type
Article
- DOI
10.1159/000502861