AlG3 Induces AURKA to Promote Laryngeal Squamous Cell Carcinoma Metastasis

Objectives To investigate the relationship between ALG3 and AURKA, the expression and potential prognostic value of ALG3 in LSCC, and to then explore the impact of ALG3 in tumorigenic effects.Methods Co-immunoprecipitation assay was detected the relationship between ALG3 and AURKA, Rt-PCR and Western blot was detected the expression of related mRNA and proteins. CCK8 assay, plate colony formation assay Cells, wound healing, migration and invasion assays were used to examine the ability of proliferation, movement, migration and invasion of LSCC cells.Results ALG3 immediately induced AURKA to promote LSCC metastasis. Moreover, ALG3 highly expressed in LSCC tissues and cells and the expression of ALG3 was positively related to tumor size, lymphatic metastasis and poor clinical prognosis. Furthermore, knockdown ALG3 in LSCC cells remarkably restrain cellular proliferation, migration and invasion in vitro and vivo.Conclusion AlG3 induced AURKA to promote LSCC metastasis and ALG3 maybe potential prognostic value for LSCC.Brief AbstractAlG3 induces AURKA to promote laryngeal squamous cell carcinoma metastasis

Identification of Novel Prognostic Markers Associated With Laryngeal Squamous Cell Carcinoma Using Comprehensive Analysis

BackgroundLaryngeal squamous cell carcinoma (LSCC) is a leading malignant cancer of the head and neck. Patients with LSCC, in which the cancer has infiltrated and metastasized, have a poor prognosis. Therefore, there is an urgent need to identify more potential targets for drugs and biomarkers for early diagnosis.MethodsRNA sequence data from LSCC and patients’ clinical traits were obtained from the Gene Expression Omnibus (GEO) (GSE142083) and The Cancer Genome Atlas (TCGA) database. Differentially expressed gene (DEG) analysis and weighted gene co-expression network analysis (WGCNA) were performed to identify hub genes. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, prognostic value analysis, receiver operating characteristic (ROC) curve analysis, gene mutation analysis, tumor-infiltrating immune cell abundance profile estimation, gene set variation analysis (GSVA), and gene set enrichment analysis (GSEA) were performed. Single-gene RNA sequencing data were obtained from the GSE150321 dataset. Cell proliferation and viability were confirmed by the CCK-8 assay and real-time PCR.ResultsA total of 701 DEGs, including 329 upregulated and 372 downregulated genes, were screened in the GSE142083 dataset. Using WGCNA, three modules were identified to be closely related to LSCC. After intersecting the DEGs and performing univariate and multivariate Cox analyses, a novel prognostic model based on three genes (SLC35C1, HOXB7, and TEDC2) for LSCC was established. Interfering TEDC2 expression inhibited tumor cell proliferation and migration.ConclusionsOur results show that SLC35C1, HOXB7, and TEDC2 have the potential to become new therapeutic targets and prognostic biomarkers for LSCC.

NK4 Regulates Laryngeal Squamous Cell Carcinoma Cell Properties and Inhibits Tumorigenicity by Modulating the DKK1/Wnt/β-Catenin Axis

ObjectiveTo investigate the effects of NK4 gene on the properties and tumorigenicity in laryngeal squamous cell carcinoma cell.MethodsHere, we used the attenuated Salmonella carrying the NK4 gene to transfect the AMC-HN-8 cells and detected the expression of NK4 by the real-time quantitative polymerase chain reaction (q RT-PCR). The properties of NK4 gene was determined by MTT method, cell scratch test, and flow cytometry. A nude mouse tumorigenesis model was used to evaluate the effect of NK4 gene on the growth of AMC-HN-8 cells in vivo. While a western blot assay was used to assess the expression of DKK1, Wnt1 and β-Catenin in nude mouse tumors.ResultsqRT-PCR showed that the expression of NK4 in the transfection group was significantly higher than that in the control group (P<0.01), and the expression increased with the time of transfection. MTT results showed NK4 overexpression inhibited the proliferation of AMC-HN-8 cells, and the inhibitory activity no longer increased with increasing dose when 30% expression supernatant was added (P<0.01). Scratch experiment showed that NK4 overexpression decreased the cell migration ability (P<0.01). Annexin V/PI double staining experiment showed that NK4 gene induced AMC-HN-8 cell apoptosis (P<0.01), and cell cycle arrest in S phase (P<0.01). NK4 overexpression inhibited tumor formation ability of AMC-HN-8 cells in vivo (P <0.05). WB detection showed that the expression of DKK1 increased, Wnt1 and β-Catenin protein decreased after the high expression of NK4.ConclusionsNK4 gene inhibit cell proliferation and migration, while promote cell apoptosis, and induce cell cycle arrest in S phase of laryngeal carcinoma AMC-HN-8 cells. NK4 overexpression inhibit the tumorigenesis ability of AMC-HN-8 cells, which may be related to the regulation of DKK1/Wnt1/β-Catenin signal axis.