Long non-coding RNA FAL1 regulated cell proliferation through Akt pathway via targeting PDK1 in esophageal cancer cells

X.-S. Liang, Y. Sun, T. Liu

Department of Cardio-Thoracic Surgery, The Second Affiliated Hospital of Guangxi Medical University, Guangxi, China. liutao1256@yeah.net

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• Oncology

OBJECTIVE: Esophageal cancer (EC) is one of the most common cancers in the world. Long non-coding RNA focally amplified lncRNA on chromosome 1 (FAL1) is an oncogene which is frequently and focally amplified in human cancers. However, the role of FAL1 in EC remains unknown. The aim of the present study was to evaluate the effect of FAL1 on EC cell lines and explore the underlying mechanism.

PATIENTS AND METHODS: The expression levels of FAL1 in EC tissues and cell lines were detected by RT-PCR. Then, Eca109 cell, a human esophageal cancer cell line, was transfected with FAL1-overexpressing vector or FAL1-siRNA or empty vector. The cell proliferation was measured by MTT assay. The cell apoptosis was assessed by TUNEL assay. The cell invasion was determined by transwell assay. The interaction effect between FAL1 and 3-phosphoinositide-dependent protein kinase 1 (PDK1) was evaluated by chromatin immunoprecipitation (ChIP) assay.

RESULTS: FAL1 was significantly up-regulated in EC tissues and human EC cell lines including Eca109, KYSE150, Eca9706, Kyse30, and TE-1 cells. Overexpression of FAL1 promoted cell proliferation, invasion ability, and cell cycle, but it inhibited cell apoptosis in EC cell lines. Overexpressed FAL1 activated Akt pathway via interacting with PDK1 in EC cell lines.

CONCLUSIONS: FAL1 regulated cell proliferation through Akt pathway via targeting PDK1 in EC cells. These findings revealed that FAL1 exhibited oncogenic activity in EC, and inhibiting FAL1 might be useful for preventing the progression of EC.

This article has been retracted. The Publisher apologizes for any inconvenience this may cause. Retraction note in: Eur Rev Med Pharmacol Sci 2024; 28 (2): 444-444.

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