Overexpression of E74‑like transformation‑specific transcription factor 3 promotes cellular proliferation and predicts poor prognosis in ovarian cancer

Abstract

E74-like E26 transformation-specific (ETS) transcription factor 3 (ELF3), is a member of the ETS transcription factor family, and has been characterized as an epithelial cell-specific transcription factor. The role of ELF3 in tumor progression remains to be elucidated. Previous studies have indicated that loss of ELF3 mRNA and protein expression was associated with poor outcomes in ovarian cancer (OC). By contrast, the present study demonstrated that ELF3 was upregulated in OC, using data from The Cancer Genome Atlas, and elevated expression levels of ELF3 were associated with a poor prognosis. ELF3 promoted OC cell proliferation in vitro and in vivo. The present study revealed that ELF3 inhibited apoptosis and reduced the cisplatin sensitivity of OC cells. Furthermore, the mTOR pathway was found to be activated by ELF3. Collectively, the results of the present study indicated the role of ELF3 in the development and pathogenesis of OC.

The ELF3 transcription factor is associated with an epithelial phenotype and represses epithelial-mesenchymal transition

“…Further, in NSCLC cells, treatment with auranofin reduced ELF3 levels and induced cell death (Lee et al ., 2021). Similarly, ELF3 overexpression in ovarian cancer cells reduced their sensitivity to cisplatin (Liu et al ., 2021). Future investigations should interrogate the coupled dynamics of ELF3, EMT and resistance to specific therapies, similar to our observations that ELF3 is associated with an epithelial and tamoxifen-resistant cell-state.…”

Hypoxia‐induced ELF3 promotes tumor angiogenesis through IGF1/IGF1R

“…In recently published papers, ELF3 was considered to be a key biomarker to diagnose and predict ovarian serous cancer (Xu et al , 2021 ; Zhang et al , 2021 ). ELF3 overexpression is reported to promote the pathogenesis of OC through the mTOR signaling pathway and induce cisplatin resistance in OCs (Liu et al , 2021 ). Furthermore, ELF3 is also known to promote OC cell growth and metastasis by inhibiting miR‐485‐5p transcription, which interferes with the CLDN4/Wnt/β‐catenin axis (Kuang & Li, 2021 ).…”