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Long intergenic non‑coding RNA 01232 (LINC01232) was identified as a critical regulator of the development of pancreatic adenocarcinoma. The present study investigated the expression and regulatory roles of LINC01232 in esophageal squamous cell carcinoma (ESCC). The main aim of the present study was to elucidate the underlying mechanisms through which LINC01232 affects the malignancy of ESCC. Initially, LINC01232 expression in ESCC was analyzed using the TCGA and GTEx databases and was confirmed using reverse transcription‑quantitative polymerase chain reaction. ESCC cell proliferation, apoptosis and migration and invasion were assessed using the Cell Counting kit‑8 assay, flow cytometric analysis, and migration and invasion assays, respectively. ESCC tumor growth in vivo was examined using a xenograft mouse model. As shown by the results, a high LINC01232 expression was detected in ESCC tissues and cell lines. LINC01232 downregulation suppressed the proliferation, migration and invasion of ESCC cells, and promoted cell apoptosis in vitro. In addition, LINC01232 depletion restricted tumor growth in vivo. Mechanistically, LINC01232 was shown to function as an microRNA‑654‑3p (miR‑654‑3p) sponge in ESCC cells, and hepatoma‑derived growth factor (HDGF) was identified as a direct target of miR‑654‑3p. LINC01232 could bind competitively to miR‑654‑3p and decrease its expression in ESCC cells, thereby promoting HDGF expression. Rescue experiments reconfirmed that the effects of LINC01232 deficiency in ESCC cells were restored by increasing the output of the miR‑654‑3p/HDGF axis. On the whole, the present study demonstrates that LINC01232 plays a tumor‑promoting role during the progression of ESCC by regulating the miR‑654‑3p/HDGF axis. The LINC01232/miR‑654‑3p/HDGF pathway may thus provide a novel theoretical basis for the management of ESCC.

international journal of molecular medicine

Long intergenic non‑coding RNA LINC01232 contributes to esophageal squamous cell carcinoma progression by sequestering microRNA‑654‑3p and consequently promoting hepatoma‑derived growth factor expression