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Int J Biochem Cell Biol. 2018 Jan;94:98-106. doi: 10.1016/j.biocel.2017.12.002. Epub 2017 Dec 5.

Overexpression of ELF3 facilitates cell growth and metastasis through PI3K/Akt and ERK signaling pathways in non-small cell lung cancer.

Author information

1
Department of Radiation Oncology, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510150, China.
2
Department of Respiratory medicine, The Second Affiliated Hospital of Guangzhou Medical University,Guangzhou,510260, China.
3
Department of Otorhinolaryngology of Nanfang Hospital,Southern Medical University, Guangzhou, 510515, China.
4
Department of General Surgery, Sun Yet-sen Memorial Hospital of Sun Yet-sen University, Guangzhou, 510120, China.
5
Department of Ultrasound, Dongguan People's Hospital Affiliated to Southern Medical University, Dongguan, 523059, Guangdong, China. Electronic address: dingshangwei_1980@163.com.
6
Department of Radiation Oncology, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510150, China. Electronic address: zhangjinshan_1966@163.com.

Abstract

ELF3 is one of the member of transcription factors from E-twenty-six family, its role varies in different types of cancer. However, the role and specific mechanisms of ELF3 in the development of non-small cell lung cancer (NSCLC) still remains largely unknown. In our study, ELF3 was observed to be upregulated in NSCLC tissues compared to the corresponding normal lung tissue at mRNA and protein levels, and its expression level was correlated with the overall survival of patients with NSCLC. Silencing of the ELF3 gene in NSCLC cells inhibited the proliferation and metastasis significantly in vitro and in vivo. Conversely, overexpression of ELF3 in NSCLC cells promoted cancer growth and metastasis in vitro. Mechanistically, ELF3 activated PI3K/AKT and ERK signaling pathways and its downstream effectors, thus regulating the cell cycle and epithelial-mesenchymal transition (EMT). Furthermore, the promotive effects of ELF3 on cellular proliferation and metastasis could be rescued by Ly294002 (inhibitor of PI3K) and U0126 (inhibitor of MEK1/2). The results show that ELF3 promotes cell growth and metastasis by regulating PI3K/Akt and ERK pathways in NSCLC and that it may be a promising new target for the treatment of NSCLC patients.

KEYWORDS:

Cell growth; ELF3; EMT; ERK; Metastasis; NSCLC; PI3K/Akt

PMID:
29208568
DOI:
10.1016/j.biocel.2017.12.002
[Indexed for MEDLINE]
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