Abstract
BackgroundTerminal differentiation-induced ncRNA (TINCR) plays an essential role in epidermal differentiation and is involved in the development of various cancers.MethodsqPCR was used to detect the expression level of TINCR in tissues and cell lines of laryngeal squamous cell carcinoma (LSCC). The potential targets of TINCR were predicted by the bioinformation website. The expression of miR-210 and BTG2 genes were detected by qPCR, and the protein levels of BTG2 and Ki-67 were evaluated by western blot. CCK-8 assay, scratch test, and transwell chamber were used to evaluate the proliferation, invasion, and metastasis ability of LSCC cells. The relationships among TINCR, miR-210, and BTG2 were investigated by bioinformatics software and luciferase reporter assay. The in vivo function of TINCR was accessed on survival rate and tumor growth in nude mice.ResultsWe used qRT-PCR to detect the expression of TINCR in laryngeal squamous cell carcinoma (LSCC) tissues and cells and found significantly lower levels in cancer tissues compared with adjacent tissues. Additionally, patients with high TINCR expression had a better prognosis. TINCR overexpression was observed to inhibit the proliferation and invasion of LSCC cells. TINCR was shown to exert its antiproliferation and invasion effects by adsorbing miR-210, which significantly promoted the proliferation and invasion of laryngeal squamous cells. Overexpression of miR-210 was determined to reverse the tumour-suppressive effects of TINCR. BTG2 (anti-proliferation factor 2) was identified as the target gene of miR-210, and BTG2 overexpression inhibited the proliferation and invasion of LSCC cells. BTG2 knockdown relieved the inhibitory effects of TINCR on the proliferation and invasion of LSCC. Finally, TINCR upregulation slowed xenograft tumour growth in nude mice and significantly increased survival compared with control mice.ConclusionThe results of this study suggest that TINCR inhibits the proliferation and invasion of LSCC by regulating the miR-210/BTG2 pathway, participates in cell cycle regulation, and may become a target for the treatment of LSCC.
Highlights
Terminal differentiation-induced non-coding RNAs (ncRNAs) (TINCR) plays an essential role in epidermal differentiation and is involved in the development of various cancers
Downregulation of Terminal differentiation-induced ncRNA (TINCR) expression in laryngeal squamous cell carcinoma (LSCC) Gene expression in tissue samples from LSCC patients was detected by RT-PCR
TINCR expression was significantly decreased in LSCC tissues compared with adjacent tissues (Fig. 1A)
Summary
Terminal differentiation-induced ncRNA (TINCR) plays an essential role in epidermal differentiation and is involved in the development of various cancers. Laryngeal cancer is an aggressive head and neck tumour. Laryngeal cancer is one of the most common malignant tumours of the head and neck [1]. The initiation and development of laryngeal cancer is a biological process involving multiple factors. With the completion of the human genome sequence, researchers have found that in addition to traditional genes, the genome is composed of more than 90% “dark matter”, which includes non-coding RNAs (ncRNAs), of which long noncoding RNAs (lncRNAs) were recently shown to be involved in the occurrence and progression of laryngeal cancer [2, 3]. Most lncRNAs cannot encode proteins but have rich biological functions. In the progression of human LSCC, abnormal lncRNA expression is often closely associated with prognosis. Qu et al found that abnormally high expression of hoxa11-as is often seen in LSCC tissues, and patients with high hoxa11-as expression tend to have a poor prognosis [6]
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