LINC00514 promotes lipogenesis and tumor progression in esophageal squamous cell carcinoma by sponging miR‑378a‑5p to enhance SPHK1 expression.

Increasing evidence has demonstrated that long non‑coding RNAs serve pivotal roles in tumor development, progression, metastasis and metabolism. However, to the best of our knowledge, the roles and molecular mechanisms of long intergenic nonprotein‑coding RNA 00514 (LINC00514) in esophageal squamous cell carcinoma (ESCC) remain unknown. The present study found that LINC00514 and sphingosine kinase 1 (SPHK1) were both upregulated in ESCC tissues and cells, and their high expression levels were closely associated with Tumor‑Node‑Metastasis stage, lymph node metastasis and poor prognosis of patients with ESCC. Functionally, knockdown of LINC00514 inhibited cell proliferation and invasion, and led to the downregulation of lipogenesis‑related proteins, including SPHK1, fatty acid synthase, acetyl‑coenzyme (Co)A carboxylase α and stearoyl‑CoA desaturase 1, whereas LINC00514 overexpression promoted cell proliferation and invasion in ESCC KYSE150 and KYSE30 cells, and upregulated expression of lipogenesis‑related proteins. Mechanistically, LINC00514 functioned as a competing endogenous RNA by sponging microRNA (miR)‑378a‑5p, resulting in the upregulation of SPHK1, which was accompanied by the activation of lipogenesis‑related pathways, to promote ESCC cell proliferation and invasion. Taken together, these findings suggest that LINC00514 may participate in ESCC lipogenesis, and targeting the LINC00514/miR‑378a‑5p/SPHK1 signaling axis may be a novel and promising therapeutic strategy for management of patients with ESCC.