Identification of an immune-related signature as a prognostic classifier for patients with early-stage head and neck squamous cell carcinoma.

Background: Head and neck squamous cell carcinoma (HNSCC) is the most common type and accounts for 90% of all head and neck cancer cases. Despite advances in early diagnosis and treatment strategies-chemotherapy, surgical resection, and radiotherapy-5-year survival remains grim. For patients with early-stage HNSCC, accurately predicting clinical outcomes is challenging. Considering the pivotal role of the immune system in HNSCC, we developed a reliable immune-related gene signature (IRGS) and explored its predictive accuracy in patients with early-stage HNSCC. Methods: We examined immune gene expression profiles and clinical information from 230 early-stage HNSCC specimens, including 100 cases from The Cancer Genome Atlas (TCGA), 49 cases from the Gene Expression Omnibus (GEO; GSE65858), and 81 cases from an independent clinical cohort. The prognostic signature was constructed using Kaplan-Meier analysis and the least absolute shrinkage and selection operator (LASSO) Cox algorithm. We also explored the IRGS-related biological pathways and immune landscape using bioinformatics analysis. Results: A nine-immune-gene signature was generated to significantly stratify patients into high and low-risk groups. High risk patients exhibited shorter survival time [hazard ratio (HR) =13.795, 95% confidence interval (CI): 3.275-58.109, P<0.001]. The signature demonstrated robust prognostic ability in the training and validation sets and could independently predict overall survival (OS) and relapse-free survival (RFS). Subsequently, the receiver operating characteristic (ROC) curve and C-index confirmed the signature's predictive accuracy compared to clinical parameters. Additionally, cases classified as low risk showed more immune cell infiltration than high-risk cases. Conclusions: Our novel IRGS is a reliable and robust classifier for accurate patient stratification and prognostic evaluation. Future studies will attempt to affirm the signature's clinical application to early-stage HNSCC.

Mechanism of miR-340-5p in laryngeal cancer cell proliferation and invasion through the lncRNA NEAT1/MMP11 axis.

OBJECTIVES: Laryngeal cancer (LC), with a relatively rare diagnosis, is a primary malignancy originating from laryngeal mucosa. This study investigated the mechanisms of microRNA (miR)- 340-5p in LC cell proliferation and invasion. METHODS: The expression patterns of miR-340-5p, long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1), and matrix metallopeptidase 11 (MMP11) in LC cells, tissues, and para-carcinoma tissues, and human bronchial epithelial cells (HBEC) were examined via RT-qPCR. The effects of elevating or silencing miR-340-5p on LC cell proliferation and invasion were examined. The subcellular localization of lncRNA NEAT1 was determined. The binding relations among miR-340-5p, lncRNA NEAT1, and MMP11 were verified. Functional rescue experiments were designed to verify the functions of lncRNA NEAT1 and MMP11 on LC cell proliferation and invasion. Nude-mouse tumor models were established to assess the role of miR-340-5p in LC in vivo. RESULTS: miR-340-5p was under-expressed in LC, and miR-340-5p overexpression repressed LC cell proliferation and invasion. Mechanically, miR-340-5p decreased lncRNA NEAT1 stability via directly binding to lncRNA NEAT1 and thus declined lncRNA NEAT1 expression in LC cells, while lncRNA NEAT1 accelerated MMP11 transcription via binding to heat shock factor 1 (HSF1). Overexpression of lncRNA NEAT1 or MMP11 reversed the repression of miR-340-5p overexpression on LC cell proliferation and invasion. In vivo, miR-340-5p overexpression repressed the tumor growth. CONCLUSION: miR-340-5p overexpression reduced lncRNA NEAT1 stability via binding to lncRNA NEAT1, which declined lncRNA NEAT1 expression and reduced the binding of lncRNA NEAT1 to HSF1 to further inhibit MMP11 transcription, thus repressing LC cell proliferation and invasion.

Athlete Behavior Recognition Technology Based on Siamese-RPN Tracker Model.

With the rapid development of deep learning algorithms, it is gradually applied in UAV (Unmanned Aerial Vehicle) driving, visual recognition, target tracking, behavior recognition, and other fields. In the field of sports, many scientists put forward the research of target tracking and recognition technology based on deep learning algorithms for athletes' trajectory and behavior capture. Based on the target tracking algorithm, a regional proposal network RPN algorithm combined with the twin regional proposal network Siamese algorithm is proposed to study the tracking and recognition technology of athletes' behavior. Then, the adaptive updating network is used to track the behavior target of athletes, and the simulation model of behavior recognition is established. This algorithm is different from the traditional twin network algorithm. It can accurately take the athlete's behavior as the target candidate box in model training and reduce the interference of environment and other factors on model recognition. The results show that the Siamese-RPN algorithm can reduce the interference from the background and environment when tracking the athletes' target behavior trajectory. This algorithm can improve the training behavior recognition model, ignore the background interference elements of the behavior image, and improve the accuracy and overall performance of the model. Compared with the traditional twin network method for sports behavior recognition, the Siamese-RPN algorithm studied in this paper can perform offline operations and distinguish the interference factors of athletes' background environment. It can quickly capture the characteristic points of athletes' behavior as the data input of the tracking model, so it has excellent popularization and application value.

miR-506 is a YAP1-dependent tumor suppressor in laryngeal squamous cell carcinoma.

Laryngeal squamous cell carcinoma (LSCC) accounts for 95% of laryngeal cancer incidence. Tobacco use has been shown to have a linear association with the development of the disease. While early diagnosis and treatment of LSCC are critical in improving the 5-year survival rate and quality of life, diagnosis of early-stage LSCC remains challenging because of the unapparent symptoms. Here, we report that miR-506, a critical regulator in many types of cancers, is aberrantly suppressed in LSCC patient tissues and cultured cancer cells. This is likely responsible for the enhanced production of YAP1 protein, a transcriptional factor that is well known for its oncogenic roles in LSCC malignancy. Statistical analysis has confirmed that the expression levels of miR-506 and YAP1 are strongly correlated with the malignant statuses of patient tumors. Restoring the expression level of miR-506 in cultured LSCC cells significantly inhibited proliferation, migration and invasion of the cells. The miR-506 and YAP1 regulatory network seems to affect at least pathways involved in apoptosis. Our study, for the first time, has demonstrated a tumor suppressive role of miR-506 in LSCC. This opens new opportunities for further exploring the molecular details of the development of the disease and thus will facilitate the development of novel diagnosis and therapeutic strategies.

Long noncoding RNA HOXC13-AS positively affects cell proliferation and invasion in nasopharyngeal carcinoma via modulating miR-383-3p/HMGA2 axis.

Long noncoding RNAs have been reported to be important regulators in numerous cancers. In this study, we found that HOXC13 antisense RNA (HOXC13-AS) was highly expressed in head and neck squamous carcinoma (HNSC) tissues in The Cancer Genome Atlas database. Nasopharyngeal carcinoma (NPC) belongs to HNSC. Therefore, we further investigated the potential role of HOXC13-AS in NPC. Quantitative reverse transcription polymerase chain reaction examination revealed that HOXC13-AS was markedly upregulated in NPC tissues and cell lines. Furthermore, HOXC13-AS was identified as an independent prognosis factor by Cox regression analyses. Subsequently, functional assay revealed that knockdown of HOXC13-AS impaired cell proliferation, migration, and invasion. Mechanistically, RIP and luciferase reporter analysis confirmed that miR-383-3p was a target of HOXC13-AS. Besides, high mobility group AT-hook 2 (HMGA2) was proved to be a target of miR-383-3p in NPC. Finally, rescue assays demonstrated that HOXC13-AS functioned as a competing endogenous RNAs to enhance the expression of HMGA2 via sponging miR-383-3p. This study suggested that HOXC13-AS exerted oncogenic function in NPC via regulating miR-383-3p/HMGA2 axis, indicating HOXC13-AS may be a potential therapeutic target for patients with NPC.