LINC01535 promotes proliferation and inhibits apoptosis in esophageal squamous cell cancer by activating the JAK/STAT3 pathway

Y. Fang, S. Zhang, J. Yin, Y.-X. Shen, H. Wang, X.-S. Chen, H. Tang

Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China. fang.yong1@zs-hospital.sh.cn

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• Oncology

OBJECTIVE: To detect the expression of long intergenic non-coding ribonucleic acid (LINC) 01535 in esophageal squamous cell cancer (ESCC) tissues and cells, and to investigate the influences of LINC01535 on the proliferation and apoptosis of ESCC cells and the possible mechanism.

PATIENTS AND METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine the relative expression of LINC01535 in 43 cases of ESCC tissues and human esophageal cancer cells (KYSE30, EC9706, TE-13, and Ecal09) compared with human esophageal mucosal epithelial cells (HET-1A). The esophageal cancer cells with the highest expression were selected and transfected with small interfering RNA (si)-LINC01535 (experimental group) or si-negative control (NC) (control group). The interference efficiency was measured via qRT-PCR assay. Regulatory effects of LINC01535 on cell proliferative capacity was examined through colony formation assay and cell proliferation assay [Cell Counting Kit-8 (CCK-8)]. Cell cycle and apoptosis influenced by LINC01535 were detected via flow cytometry. Western blotting was applied to determine the expression changes in the molecular markers of the Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) signaling pathway.

RESULTS: LINC01535 expression in ESCC tissues and cells was remarkably higher than that in para-carcinoma tissues and esophageal mucosal epithelial cells. Knockdown of LINC01535 decreased proliferative capacity, arrested cell cycle in G1/G0 phase, and increased apoptotic rate of ESCC cells. The expressions of the molecular markers of the JAK/STAT3 signaling pathway were altered after knockdown of LINC01535. The above results illustrated that LINC01535 accelerated the proliferation but repressed the apoptosis of ESCC cells by regulating the JAK/STAT3 signaling pathway.

CONCLUSIONS: The expression of LINC01535 is up-regulated in ESCC tissues and cells, and the highly expressed LINC01535 promotes the proliferation and inhibits the apoptosis of ESCC cells by regulating the JAK/STAT3 signaling pathway. Our findings provide new directions for the diagnosis and treatment of esophageal cancer.

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