Abstract

Aberrant expression of LINC00520 has been identified in head and neck squamous carcinoma (HNSCC). However, its function in the radiosensitivity of HNSCC remain unclear. Herein, we aimed to define the role LINC00520 in the radiosensitivity of HNSCC and identify the underlying mechanism. Tumour tissues and adjacent normal tissue were collected from HNSCC patients. Differentially expressed genes (DEGs) in HNSCC tumour were obtained from the cancer genome atlas (TCGA) database. Interactions between LINC00520 and miR-195, homeobox A10 (HOXA10) and miR-195 were evaluated by dual-luciferase reporter gene assay, RNA Immunoprecipitation (RIP), and RNA pull-down assay. The effects of LINC00520/miR-195/HOXA10 on radiosensitivity of HNSCC were analysed in the evaluation of radiotherapy outcome. Cell proliferation, invasion, migration, and apoptosis of HNSCC cells were accessed via gain- and loss-of-function approaches. Tumour xenograft in nude mice was conducted in order to confirm the results in vivo. LINC00520 was upregulated while miR-195 was downregulated in HNSCC cells and tissues. Silencing LINC00520 or overexpressing miR-195 promoted radiosensitivity and inhibited cell proliferation, invasion, migration, and apoptosis in HNSCC. Moreover, these in vitro findings were reproduced in vivo in human HNSCC xenograft in nude mice. LINC00520/miR-195/HOXA10 is involved in the radiosensitivity mediation, providing potential therapeutic target for HNSCC treatment.

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