Abstract
Long non-coding RNA (lncRNA) FEZF1 antisense RNA 1 (FEZF1-AS1) has been shown to be up-regulated in tumor tissues and cells, and exerts oncogenic effects on various types of malignancies. However, the expression and function of FEZF1-AS1 was still fully unclear in retinoblastoma. The purpose of our study was to investigate the expression and clinical value of FEZF1-AS1 in retinoblastoma patients, and explore the effect of FEZF1-AS1 on retinoblastoma cell proliferation, migration and invasion. In our results, levels of FEZF1-AS1 expression were elevated in retinoblastoma tissue specimens and cell lines compared with adjacent normal retina tissue specimens and human retinal pigment epithelial cell line, respectively. The correlation analysis indicated that high FEZF1-AS1 expression was significantly correlated with present choroidal invasion and optic nerve invasion. Survival analysis suggested that retinoblastoma patients in high FEZF1-AS1 expression group had obviously short disease-free survival (DFS) compared with retinoblastoma patients in low FEZF1-AS1 expression group, and high FEZF1-AS1 expression was an independent unfavorable prognostic factor for DFS in retinoblastoma patients. Loss-of-function study indicated silencing FEZF1-AS1 expression inhibited retinoblastoma cell proliferation, invasion and migration. In conclusion, FEZF1-AS1 functions as an oncogenic lncRNA in retinoblastoma.
Highlights
Retinoblastoma originated from the retinal photoreceptor precursor cells, and is the most common childhood intraocular cancer accounting for 3% of all pediatric cancers [1,2]
The results suggested that retinoblastoma tissue specimens exhibited higher FEZF1-AS1 expression than adjacent normal retina tissue specimens (Figure 1A)
In recent years, increasing studies suggested that FEZF1-AS1 was significantly overexpressed in many types of human cancers, such as lung cancer [18,19,20,21], breast cancer [22], liver cancer [23,24], gastric cancer [25,26,27], colorectal cancer [28,29], pancreatic cancer [30,31], ovarian cancer [32], cervical cancer [33], osteosarcoma [34], nasopharyngeal carcinoma [35] and multiple myeloma [36]
Summary
Retinoblastoma originated from the retinal photoreceptor precursor cells, and is the most common childhood intraocular cancer accounting for 3% of all pediatric cancers [1,2]. The incidence of retinoblastoma is about 1 case in every 15000–20000 live births [3]. The tumorigenesis of retinoblastoma is a highly complicated process, which has close relationship with gene mutation [6,7], oncogene aberrant expression [8,9], and activation of oncogenic signaling pathways [10,11]. The molecular mechanisms underlying retinoblastoma occurrence and development remain unknown. It is very useful to investigate the molecular mechanisms of retinoblastoma initiation to develop new targeted therapy and improving clinical outcome
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