Label-free quantitative proteomic analysis identifies CTNNB1 as a direct target of FOXP3 in gastric cancer cells
Corrigendum in: /10.3892/ol.2018.9017
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- Published online on: March 15, 2018 https://doi.org/10.3892/ol.2018.8277
- Pages: 7655-7660
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Copyright: © Pan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
Forkhead box protein 3 (FOXP3) is expressed in numerous types of tumor cell and is associated with tumor progression and prognosis. A previous study reported that FOXP3 inhibited cellular proliferation and induced apoptosis of gastric cancer (GC) cells by activating the apoptosis signaling pathway. In the present study, label‑free quantitative proteomic analysis and chromatin immunoprecipitation‑polymerase chain reaction (ChIP‑PCR) was performed to investigate the mechanism by which the anticancer role of FOXP3 was mediated and the proteins that with which it may interact. Label‑free quantitative proteomic analysis was used to screen for proteins differentially expressed between FOXP3‑overexpressing GC (AF) and vector (ANC) cells. Catenin β1 (CTNNB1) was one of the proteins that exhibited the greatest difference between AF and ANC among 3,313 proteins identified by liquid chromatography with tandem mass spectrometry analysis. The expression of CTNNB1 was evaluated by reverse transcription‑quantitative PCR and western blotting. The association between FOXP3 and CTNNB1 was confirmed by ChIP‑PCR in AGS cells. The changes in expression of epithelial‑mesenchymal transition‑associated proteins were analyzed by western blotting. The level of FOXP3 expression was positively associated with CTNNB1 and E‑cadherin expression, but not with vimentin and N‑cadherin expression. FOXP3 positively regulates CTNNB1 and binds to it directly. Along with the upregulation of glycogen synthase kinase 3β (GSK3β), which was also a protein whose expression was found to change significantly in proteomic analysis and has a key role in the Wnt pathway. This association is an attractive and novel hypothesis for the mechanism by which FOXP3 inhibits the invasion and metastasis of GC cells.
