Abstract 2650
Background
The functions of many long non-coding RNAs (lncRNAs) in human cancers remain to be clarified. Induction of E2F4as (antisense) by Wnt signaling may contribute to carcinogenesis by reducing levels of the E2F4as cell cycle repressor in colorectal cancer. Disruption of Wnt signaling is common in ovarian cancer. Despite the proposed models of E2F4as function, the significance of E2F4as RNA remains unclear in cancer. In this study, we examined the expression level of E2F4as in the serum of ovarian cancer patients and the functional role of E2F4as in ovarian cancer.
Methods
The serum samples were obtained from 116 pathological diagnosed ovarian cancer patients and 39 normal age-matched women. The expression of E2F4as was measured by real time RT-PCR. To investigate the role of E2F4as in cell proliferation, invasion, and migration, E2F4as expression in ovarian cancer cells was knocked down using RNA interference.
Results
The expression of E2F4as was significantly higher in the serum of ovarian cancer patients than in control patients (P < 0.05). E2F4as siRNA in SKOV3 cells decreased cell proliferation, invasion, and migration. Moreover, Knockdown of E2F4as decreased the expression of epithelial-mesenchymal transition (EMT), which are important for cell motility and metastasis. Mechanistic investigation revealed that Notch1, Hes1 and p300 proteins could be inhibited by E2F4as depletion.
Conclusions
These findings highlight the clinical significance of E2F4as in predicting the prognosis of ovarian cancer patients and suggest its potential in promoting tumor aggressiveness by regulation of the Notch signaling pathway and EMT-related mechanisms.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.
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