Long-chain non-coding RNA Linc00888 promotes the proliferation and migration of esophageal cancer cells by downregulating miR-34a expression

H.-L. Zang, Y.-H. Li, G.-M. Huang

Department of General Surgery, China-Japan Union Hospital of Jilin University, Changchun, China. huanggm@jlu.edu.cn

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• Oncology

OBJECTIVE: To explore the role and potential mechanism of long-chain non-coding RNA 00888 in esophageal cancer (EC).

PATIENTS AND METHODS: The expression level of Linc00888 in esophageal cancer tissues and adjacent ones, as well as corresponding cell lines, was measured by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Survival prognosis information of patients was collected, and KM survival analysis was performed to determine the prognostic value of Linc00888. To better understand the effect of Linc00888 on the proliferative and migration ability of EC cells, Cell Counting Kit-8 (CCK-8), clone formation, and transwell assays were performed after Linc00888 was knocked down in EC cell lines. Furthermore, bioinformatics prediction website was used to discover the potential target of Linc00888. Then, Dual-Luciferase reporter gene assay was performed to verify the binding relationship between Linc00888 and the downstream gene miR-34a. Then, the expression relationship between the two was measured both in cell lines and tissues. Finally, to clarify the regulation between Linc00888 and miR-34a, a recovery experiment was performed using co-transfection technology.

RESULTS: Linc00888 was aberrantly upregulated in esophageal cancer tissues. The survival analysis showed that the higher expression of Linc00888 was significantly correlated with shorter overall survival. Cell functional experiment results suggested that Linc00888 played a role in promoting tumor proliferative and migration ability in EC cells. Besides, Dual-Luciferase reporter genes assay indicated that miR-34a and Linc00888 had binding sites. Meanwhile, we confirmed that there was a negative correlation between the expression levels of miR-34a and Linc00888 in cells and tissues. Cellular functional recovery experiments revealed that Linc00888 could modulate the progression of EC by miR-34a.

CONCLUSIONS: Linc00888 promotes the proliferative and migration ability of EC through miR-34a.

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