Search

Background Terminal differentiation-induced ncRNA (TINCR) plays an essential role in epidermal differentiation and is involved in the development of various cancers. Methods qPCR 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. Results We 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. Conclusion The 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.

Background Laryngeal squamous cell carcinoma (LSCC) is a common malignant tumour of the head and neck. Our previous study reveals that the circular RNA (circRNA) hsa_circ_0042823 is abnormally expressed in LSCC, suggesting that hsa_circ_0042823 is closely associated with LSCC. Here, we attempted to explore the molecular mechanism of hsa_circ_0042823 in LSCC. Methods Quantitative real-time PCR and western blot were performed to assess the expression of gene and protein in human laryngeal carcinoma cells, TU212 and TU686. MTT and transwell assays were performed to examine cell proliferation, migration and invasion. The relationship among hsa_circ_0042823, miR-877-5p and forkhead box M1 (FOXM1) was verified by luciferase reporter assay. Finally, we constructed a subcutaneous tumour mouse model to analyse in vivo growth of LSCC cells following knockdown of hsa_circ_0042823. Results Compared with normal human bronchial epithelial cells (HBECs), hsa_circ_0042823 was highly expressed in the LSCC cell lines (AMC-HN-8 and TU686). Further studies demonstrated that hsa_circ_0042823 interacted with miR-877-5p, and FOXM1 was the target of miR-877-5p. Hsa_circ_0042823 promoted the expression of FOXM1 via its ceRNA activity on miR-877-5p. Hsa_circ_0042823 overexpression promoted proliferation, migration and invasion of AMC-HN-8 cells through regulating miR-877-5p/FOXM1 axis. Additionally, inhibition of hsa_circ_0042823 inhibited growth of LSCC in vivo via miR-877-5p/FOXM1 axis. Conclusions Hsa_circ_0042823/miR-877-5p/FOXM1 axis participates in the progression of LSCC. This work demonstrates that hsa_circ_0042823 accelerates cancer progression by regulating miR-877-5p/FOXM1 axis in LSCC. Therefore, this study may provide new insights into the pathogenesis of LSCC.KEY MESSAGESHsa_circ_0042823 promotes FOXM1 expression by sponging miR-877-5p.Hsa_circ_0042823 promotes proliferation, migration, invasion of LSCC cells.Hsa_circ_0042823 knockdown inhibits tumour growth of LSCC via miR-877-5p/FOXM1 axis.

Background：The HOX family transcription factor HOXB9 is a crucial element in the progression of various cancers. In the previous study conducted by the investigators, a drastically higher HOXB9 expression was reported in laryngeal squamous cell cancer (LSCC), when compared to adjacent normal laryngeal squamous tissues. Furthermore, a high level of HOXB9 was closely correlated with histological grade and overall survival in LSCC patients. However, the underlying molecular mechanisms have not been fully elucidated.Results: The present study explored the molecular mechanisms of HOXB9 in LSCC progression. Furthermore, the in vitro and in vivo studies revealed that the gene knockout of HOXB9 using the CRISPR/CAS9 system inhibited cell proliferation, migration and invasion, and promoted cell apoptosis. Mechanistic studies in LSCC cell lines and human LSCC specimens demonstrated that HOXB9 promotes LSCC progression by directly upregulating the MMP12 expression at the level of its transcription.Conclusions: Collectively, the present study is the first to demonstrate the role of HOXB9 in the regulation of LSCC progression by enhancing the upregulation of MMP12.

Background Various microRNAs (miRNAs) negatively modulate genes that are involved in cellular proliferation, differentiation, invasion, and apoptosis. In many types of cancer, the expression profiles of these miRNAs are altered. Recently, miR-101 was identified as a tumour suppressor and was found to be expressed at low levels in various types of tumours, including prostate, breast, endometrium, and bladder cancers. However, the function(s) of miR-101 in laryngeal carcinoma remain unknown. Methods The expression levels of miR-101 in laryngeal squamous cell carcinoma (LSCC) tissues and cells were detected by qPCR. Cell proliferation, migration, cell cycle, and apoptosis assay were applied to assess the function(s) of miR-101 in vitro. Nude mice subcutaneous tumour model was used to perform in vivo study. Moreover, we identified Cyclin-dependent kinase 8 (CDK8) as the target of miR-101 by a luciferase assay. The possible downstream effectors of CDK8 were investigated in Wnt/β-catenin signaling pathway. Changes of CDK8, β-catenin, and cyclin D1 protein levels were analyzed by western blotting and immunohistochemical staining. The prognostic effect of miR-101 was evaluated using the Kaplan–Meier method. Results Expression of miR-101 was down-regulated in the LSCC tissues compared with the adjacent normal tissues. Furthermore, downregulation of miR-101 correlated with T3–4 tumour grade, lymph node metastasis, and an advanced clinical stage in the LSCC patients examined (P