Background: Esophageal cancer is one of the most frequent cancers with a higher mortality worldwide. Although many long non-coding RNAs (LncRNAs) are reported to play important roles in the progression of esophageal cancer, the function of lncRNA GIHCG in esophageal cancer remains unclear.
Methods: The expression of GIHCG in esophageal cancer tissues and cancer cell lines was detected by qRT-PCR. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8) assay, EdU staining assay and colony formation assay. Cell invasion and migration were measured by transwell assay. Cell apoptosis was detected by a flow cytometer. Luciferase reporter assay and RIP assay were used to determine the interaction between GIHCG and miR-29b-3p, and their subsequent regulation of anoctamin 1 (ANO1). The expression of ANO1 in esophageal cancer tissues and cell lines was detected by Western blot. The effect of GIHCG/miR-29b-3p in tumor formation was assessed by the xenograft nude mice model in vivo.
Results: GIHCG was significantly upregulated in esophageal cancer tissues and relevant cancer cell lines. Downregulation of GIHCG significantly inhibited the growth, colony formation, invasion, migration and induced apoptosis of esophageal cancer cells in vitro. Bioinformatic analysis and RIP assay determined that GIHCG was a sponge of miR-29b-3p, and ANO1 was a direct target of miR-29b-3p. Moreover, functional experiments showed that GIHCG upregulated ANO1 expression by directly sponging miR-29b-3p. Furthermore, in vivo experiment revealed that knockdown of GIHCG significantly inhibited tumor growth in nude mice.
Conclusion: Our study revealed that lncRNA GIHCG promoted the progression of esophageal cancer by targeting the miR-29b-3p/ANO1 axis, suggesting that GIHCG might be a novel therapeutic target for esophageal cancer.
Keywords: esophageal cancer, GIHCG, miR-29b-3p, ANO1, tumorigenesis