Octamer-binding protein 4 affects the cell biology and phenotypic transition of lung cancer cells involving β-catenin/E-cadherin complex degradation

Chen,Zhong‑Shu; Ling,Dong‑Jin; Zhang,Yang‑De; Feng,Jian‑Xiong; Zhang,Xue‑Yu; Shi,Tian‑Sheng

doi:10.3892/mmr.2014.2992

Octamer-binding protein 4 affects the cell biology and phenotypic transition of lung cancer cells involving β-catenin/E-cadherin complex degradation

Authors:
- Zhong‑Shu Chen
- Dong‑Jin Ling
- Yang‑De Zhang
- Jian‑Xiong Feng
- Xue‑Yu Zhang
- Tian‑Sheng Shi
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Affiliations: Ministry of Health Hepatobiliary and Enteric Surgery Center, Xiangya School of Medicine, Central South University, Changsha, Hunan 410008, P.R. China, Department of Thoracic Surgery, Jiangxi Provincial Chest Hospital, Nanchang, Jiangxi 330006, P.R. China
Published online on: November 21, 2014 https://doi.org/10.3892/mmr.2014.2992
Pages: 1851-1858

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Abstract

Clinical studies have reported evidence for the involvement of octamer‑binding protein 4 (Oct4) in the tumorigenicity and progression of lung cancer; however, the role of Oct4 in lung cancer cell biology in vitro and its mechanism of action remain to be elucidated. Mortality among lung cancer patients is more frequently due to metastasis rather than their primary tumors. Epithelial‑mesenchymal transition (EMT) is a prominent biological event for the induction of epithelial cancer metastasis. The aim of the present study was to investigate whether Oct4 had the capacity to induce lung cancer cell metastasis via the promoting the EMT in vitro. Moreover, the effect of Oct4 on the β‑catenin/E‑cadherin complex, associated with EMT, was examined using immunofluorescence and immunoprecipitation assays as well as western blot analysis. The results demonstrated that Oct4 enhanced cell invasion and adhesion accompanied by the downregulation of epithelial marker cytokeratin, and upregulation of the mesenchymal markers vimentin and N‑cadherin. Furthermore, Oct4 induced EMT of lung cancer cells by promoting β‑catenin/E‑cadherin complex degradation and regulating nuclear localization of β‑catenin. In conclusion, the present study indicated that Oct4 affected the cell biology of lung cancer cells in vitro through promoting lung cancer cell metastasis via EMT; in addition, the results suggested that the association and degradation of the β‑catenin/E‑cadherin complex was regulated by Oct4 during the process of EMT.

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