A cuproptosis-related lncRNA signature predicts the prognosis and immune cell status in head and neck squamous cell carcinoma.

Introduction: The incidence of head and neck squamous cell carcinoma (HNSCC), one of the most prevalent tumors, is increasing rapidly worldwide. Cuproptosis, as a new copper-dependent cell death form, was proposed recently. However, the prognosis value and immune effects of cuproptosis-related lncRNAs (CRLs) have not yet been elucidated in HNSCC. Methods: In the current study, the expression pattern, differential profile, clinical correlation, DNA methylation, functional enrichment, univariate prognosis factor, and the immune effects of CRLs were analyzed. A four-CRL signature was constructed using the least absolute shrinkage and selection operator (LASSO) algorithm. Results: Results showed that 20 CRLs had significant effects on the stage progression of HNSCC. Sixteen CRLs were tightly correlated with the overall survival (OS) of HNSCC patients. Particularly, lnc-FGF3-4 as a single risk factor was upregulated in HNSCC tissues and negatively impacted the prognosis of HNSCC. DNA methylation probes of cg02278768 (MIR9-3HG), cg07312099 (ASAH1-AS1), and cg16867777 (TIAM1-AS1) were also correlated with the prognosis of HNSCC. The four-CRL signature that included MAP4K3-DT, lnc-TCEA3-1, MIR9-3HG, and CDKN2A-DT had a significantly negative effect on the activation of T cells follicular helper and OS probability of HNSCC. Functional analysis revealed that cell cycle, DNA replication, and p53 signal pathways were enriched. Discussion: A novel CRL-related signature has the potential of prognosis prediction in HNSCC. Targeting CRLs may be a promising therapeutic strategy for HNSCC.

A novel microRNA panel exhibited significant potential in evaluating the progression of laryngeal squamous cell carcinoma.

Background: Laryngeal squamous cell carcinoma (LSCC) is a common cancer of the head and neck in humans. The 5-years survival rate of patients with LSCC have declined in the past four decades. microRNAs (miRNAs) has been reported to be capable of predicting the prognosis outcomes of patients with different cancers. However, there are no reports on the usage of multi-miRNAs model as signature for the diagnosis or prognosis of LSCC. Methods: To establish the miRNAs expression-associated model for diagnosis, prognosis prediction and aided therapy of patients with LSCC, the present study enrolled 107 patients with LSCC in clinic and obtained 117 LSCC samples data from TCGA database for evaluation, respectively. Next generation sequencing (NGS), raw data processing, the least absolute shrinkage and selection operator algorithm, Cox regression analysis, construction of nomogram and cell function assays (including proliferation, migration and invasion assays) were sequentially performed. Results: There were massively dysregulated miRNAs in the LSCC compared to normal tissues. A six-miRNAs signature consists of miR-137-3p, miR-3934-5p, miR-1276, miR-129-5p, miR-7-5p and miR-105-5p was built for prognosis prediction of LSCC patients. The six-miRNAs signature is strongly associated with the poor overall survival (OS, p = 2.5e-05, HR: 4.30 [2.20-8.50]), progression free interval (PFI, p = 0.025, HR: 1.94 [1.08-3.46]) and disease specific survival (DSS, p = 1.1e-05, HR: 5.00 [2.50-10.00]). A nomogram for prediction of 2-, 3- and 5-years OS was also developed based on the six-miRNAs signature and clinical features. Furthermore, blocking the function of each of the six miRNAs inhibited proliferation, invasion and migration of LSCC cells. Conclusions: The performance of six-miRNAs signature described in the current study demonstrated remarkable potential for progression assessment of LSCC. Moreover, the six-miRNAs signature may serve as predictive tool for prognosis and therapeutic targets of LSCC in clinic.

Identification of a seven-lncRNAs panel that serves as a prognosis predictor and contributes to the malignant progression of laryngeal squamous cell carcinoma.

Background: Laryngeal squamous cell carcinoma (LSCC) is one of the most frequent head and neck cancers worldwide. Long non-coding RNAs (lncRNAs) play a critical role in tumorigenesis. However, the clinical significance of lncRNAs in LSCC remains largely unknown. Methods: In this study, transcriptome sequencing was performed on 107 LSCC and paired adjacent normal mucosa (ANM) tissues. Furthermore, RNA expression and clinical data of 111 LSCC samples were obtained from The Cancer Genome Atlas (TCGA) database. Bioinformatics analysis were performed to construct a model for predicting the overall survival (OS) of LSCC patients. Moreover, we investigated the roles of lncRNAs in LSCC cells through loss-of-function experiments. Results: A seven-lncRNAs panel including ENSG00000233397, BARX1-DT, LSAMP-AS1, HOXB-AS4, MNX1-AS1, LINC01385, and LINC02893 was identified. The Kaplan-Meier analysis demonstrated that the seven-lncRNAs panel was significantly associated with OS (HR:6.21 [3.27-11.81], p-value<0.0001), disease-specific survival (DSS) (HR:4.34 [1.83-10.26], p-value=0.0008), and progression-free interval (PFI) (HR:3.78 [1.92-7.43], p-value=0.0001). ROC curves showed the seven-lncRNAs panel predicts OS with good specificity and sensitivity. Separately silencing the seven lncRNAs inhibited the proliferation, migration, and invasion capacity of LSCC cells. Conclusion: Collectively, this seven-lncRNAs panel is a promising signature for predicting the prognosis of LSCC patients, and these lncRNAs could serve as potential targets for LSCC treatment.

FSCN1 acts as a promising therapeutic target in the blockade of tumor cell motility: a review of its function, mechanism, and clinical significance.

Fascin actin-bundling protein 1 (FSCN1) is an actin-bundling protein that is capable of inducing membrane protrusions and plays critical roles in cell migration, motility, adhesion, and other cellular interactions. FSCN1 also plays a role in forming and stabilizing filopodia or microspikes, which assist during cell migration. Furthermore, FSCN1 is a downstream target of several microRNAs and participates in various biological processes, such as epithelial-to-mesenchymal transition and autophagy, which regulate the invasion and migration ability of cells in various cancers. Increased FSCN1 levels have been associated with enhanced migration and invasion of multiple cancers as well as poor patient prognosis. Promising results from in vitro experimental studies using docosahexaenoic acid (DHA) in breast cancer and recombinant porcine NK-lysin A in hepatocellular carcinoma have revealed that anticancer drugs targeting FSCN1 have significant potential clinical applications. This review discusses FSCN1 in terms of five aspects: structure and function, biological processes, regulatory mechanisms, clinical applications, and future prospects.

An original cuproptosis-related genes signature effectively influences the prognosis and immune status of head and neck squamous cell carcinoma.

Background: Recently, a non-apoptotic cell death pathway that is dependent on the presence of copper ions was proposed, named as cuproptosis. Cuproptosis have been found to have a strong association with the clinical progression and prognosis of several cancers. Head and neck squamous cell carcinoma (HNSC) are among the most common malignant tumors, with a 5-year relative survival rate ranging between 40% and 50%. The underlying mechanisms and clinical significance of cuproptosis-related genes (CRGs) in HNSC progression have not been clarified. Methods: In this study, expression pattern, biological functions, Immunohistochemistry (IHC), gene variants and immune status were analyzed to investigate the effects of CRGs on HNSC progression. Moreover, a 12-CRGs signature and nomogram were also constructed for prognosis prediction of HNSC. Results: The results revealed that some CRGs were dysregulated, had somatic mutations, and CNV in HNSC tissues. Among them, ISCA2 was found to be upregulated in HNSC and was strongly correlated with the overall survival (OS) of HNSC patients (HR = 1.13 [1.01-1.26], p-value = 0.0331). Functionally, CRGs was mainly associated with the TCA cycle, cell cycle, iron-sulfur cluster assembly, p53 signaling pathway, chemical carcinogenesis, and carbon metabolism in cancer. A 12-CRGs signature for predicting the OS was constructed which included, CAT, MTFR1L, OXA1L, POLE, NTHL1, DNA2, ATP7B, ISCA2, GLRX5, NDUFA1, and NDUFB2. This signature showed good prediction performance on the OS (HR = 5.3 [3.4-8.2], p-value = 3.4e-13) and disease-specific survival (HR = 6.4 [3.6-11], p-value = 2.4e-10). Furthermore, 12-CRGs signature significantly suppressed the activation of CD4+ T cells and antigen processing and presentation. Finally, a nomogram based on a 12-CRGs signature and clinical features was constructed which showed a significantly adverse effect on OS (HR = 1.061 [1.042-1.081], p-value = 1.6e-10) of HNSC patients. Conclusion: This study reveals the association of CRGs with the progression of HNSC based on multi-omics analysis. The study of CRGs is expected to improve clinical diagnosis, immunotherapeutic responsiveness and prognosis prediction of HNSC.

Application of the CRISPR/Cas9-based gene editing technique in basic research, diagnosis, and therapy of cancer.

The 2020 Nobel Prize in Chemistry was awarded to Emmanuelle Charpentier and Jennifer Doudna for the development of the Clustered regularly interspaced short palindromic repeats/CRISPR-associated nuclease9 (CRISPR/Cas9) gene editing technology that provided new tools for precise gene editing. It is possible to target any genomic locus virtually using only a complex nuclease protein with short RNA as a site-specific endonuclease. Since cancer is caused by genomic changes in tumor cells, CRISPR/Cas9 can be used in the field of cancer research to edit genomes for exploration of the mechanisms of tumorigenesis and development. In recent years, the CRISPR/Cas9 system has been increasingly used in cancer research and treatment and remarkable results have been achieved. In this review, we introduced the mechanism and development of the CRISPR/Cas9-based gene editing system. Furthermore, we summarized current applications of this technique for basic research, diagnosis and therapy of cancer. Moreover, the potential applications of CRISPR/Cas9 in new emerging hotspots of oncology research were discussed, and the challenges and future directions were highlighted.

Regulatory role and mechanism of m6A RNA modification in human metabolic diseases.

Metabolic diseases caused by disorders in amino acids, glucose, lipid metabolism, and other metabolic risk factors show high incidences in young people, and current treatments are ineffective. N 6-methyladenosine (m6A) RNA modification is a post-transcriptional regulation of gene expression with several effects on physiological processes and biological functions. Recent studies report that m6A RNA modification is involved in various metabolic pathways and development of common metabolic diseases, making it a potential disease-specific therapeutic target. This review explores components, mechanisms, and research methods of m6A RNA modification. In addition, we summarize the progress of research on m6A RNA modification in metabolism-related human diseases, including diabetes, obesity, non-alcoholic fatty liver disease, osteoporosis, and cancer. Furthermore, opportunities and the challenges facing basic research and clinical application of m6A RNA modification in metabolism-related human diseases are discussed. This review is meant to enhance our understanding of the molecular mechanisms, research methods, and clinical significance of m6A RNA modification in metabolism-related human diseases.

Epidemiological Analysis of 1234 Cases of Laryngeal Cancer in Shanxi Province, China.

BACKGROUND: Laryngeal cancer is a common malignancy of the head and neck, especially in northern China, including Shanxi province. This study intends to describe the epidemiological characteristics of laryngeal cancer in Shanxi Province, China, in order to support prevention and treatment efforts. METHODS: Retrospective analysis of the medical records of patients diagnosed with laryngeal cancer in hospitals in Shanxi Province from 2008 to 2012. RESULTS: The average annual incidence rate of laryngeal cancer in Shanxi province from 2008 to 2012 was 0.70/105, the Chinese population standardized incidence rate was 0.57/105 and the world population standardized incidence rate was 0.60/105. The city with the highest incidence of laryngeal cancer in Shanxi Province is Taiyuan, followed by Yangquan, and the lowest incidence are Yuncheng and Jincheng. The cases included 723 farmers (58.6%), 338 workers (27.4%), 95 government cadres (7.7%), 35 unemployed individuals (2.8%), 30 teachers (2.4%) and 13 individuals with other occupations (1.1%). The incidence of laryngeal cancer in rural areas was 0.78/105, while urban areas was 0.60/105. Of 1006 patients with smoking and drinking status reported, there were 238 both smoking and drinking (23.7%), 491 only smoking but not drinking (48.8%), 4 only drinking but not smoking (0.4%), 273 both not smoking and not drinking (27.1%) (P<0.001), and there were 695 males smoking (95.3%), 34 females smoking (4.7%) (P<0.001). Of 879 patients for whom the primary cancer location was known, 406 cases (46.2%) were supraglottic and 428 cases (48.7%) were glottic. Among 1009 patients with known pathological classification, the vast majority had squamous cell carcinoma (992 cases, 98.3%). CONCLUSIONS: To sum up, the incidence of laryngeal cancer in Shanxi Province exhibited a relatively stable trend from 2008 to 2012, and the incidence is higher in men than in women in all years. The high percentage of smokers in this study underscores the importance of smoking as a risk factor for laryngeal cancer, whereas rates of drinking did not appear to be linked. Incidence of laryngeal cancer was higher in rural areas than in urban areas, a pattern that differs from other regions of China and internationally.

miR-1207-5p suppresses laryngeal squamous cell carcinoma progression by downregulating SKA3 and inhibiting epithelial-mesenchymal transition.

Laryngeal squamous cell carcinoma (LSCC) is the second most common head and neck cancer. Previously, we discovered that miR-1207-5p was downregulated in LSCC. In this study, the clinical significance, function, and mechanism of miR-1207-5p in LSCC were investigated. Downregulation of miR-1207-5p was found to be strongly linked to the malignant progression of LSCC. Functional studies revealed that miR-1207-5p upregulation suppressed LSCC cell proliferation, invasion, migration, and xenograft tumor growth. Bioinformatics analysis revealed that miR-1207-5p target genes were involved in cell cycle regulation, proliferation, adhesion, and the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Mechanistic studies revealed that miR-1207-5p interacts directly with the 3' untranslated region of spindle and kinetochore associated complex subunit 3 (SKA3) and downregulates SKA3 expression. Furthermore, SKA3 was found to be overexpressed in LSCC, and its high expression was associated with tumor progression and a poor prognosis. Rescue experiments demonstrated that miR-1207-5p inhibited the malignant phenotypes of LSCC via SKA3. Furthermore, miR-1207-5p upregulation or knockdown of SKA3 inhibited the epithelial-mesenchymal transition (EMT). Collectively, miR-1207-5p inhibited LSCC malignant progression by downregulating SKA3 and preventing EMT. These findings provide new insights into the mechanism of LSCC progression, as well as new potential biomarkers and therapeutic targets for LSCC diagnosis and treatment.

Tumor microenvironment and immune-related therapies of head and neck squamous cell carcinoma.

Head and neck squamous cell carcinomas (HNSCCs) are a type of common malignant tumor, mainly manifesting as oropharyngeal, oral cavity, laryngopharyngeal, hypopharyngeal, and laryngeal cancers. These highly aggressive malignant tumors reportedly affect more than 830,000 patients worldwide every year. Currently, the main treatments for HNSCC include surgery, radiotherapy, chemotherapy, and immunotherapy, as well as combination therapy. However, the overall 5-year survival rate of HNSCC has remained 50%, and it has not significantly improved in the past 10 years. Previous studies have shown that the tumor microenvironment (TME) plays a crucial role in the recurrence, metastasis, and drug resistance of patients with HNSCC. In this review, we summarize the role of anti-tumor and pro-tumor immune cells, as well as extracellular components in the TME of HNSCC. We also discuss classical HNSCC immunotherapy and highlight examples of clinical trials using CTLA-4 inhibitors and programmed cell death 1 (PD-1)/programmed cell death ligand 1 (PD-L1)-related combination therapies. We also outline some molecules in the TME known to regulate immunosuppressive cells. Furthermore, the role and underlying mechanism of radiation therapy on the TME, immune cells, and immune response are discussed.

Petroleum extract of Farfarae Flos alleviates nasal symptoms by regulating the Th1-Th2 cytokine balance in a mouse model of Allergic Rhinitis.

Farfarae Flos is a traditional Chinese medicine that has long been used to treat allergies. In this study, we aimed to investigate the effect of a petroleum extract of Farfarae Flos (PEFF) in a mouse model of allergic rhinitis (AR) and to explore the underlying molecular mechanisms of action. An animal model of AR was established by sensitization and challenge of BALB/c mice with ovalbumin (OVA). PEFF was administered intranasally and AR nasal symptoms were assessed on a semi-quantitative scale according to the frequencies of nose rubbing and sneezing and the degree of rhinorrhea. The mechanism of action of PEFF was evaluated by histological analysis of nasal mucosa architecture and inflammatory status; ELISA-based quantification of serum OVA-specific IgE, interferon-γ (IFN-γ), and interleukin-4 (IL-4) concentrations; and immunohistochemical and western blot analysis of T-bet and GATA3 protein expression in nasal mucosa and spleen tissues. The results showed intranasal administration of PEFF alleviated AR symptom scores and reduced both the infiltration of inflammatory cells and tissue damage in the nasal mucosa. PEFF significantly decreased serum concentrations of OVA-specific IgE (P<0.01) and IL-4 (P<0.05) and significantly increased IFN-γ (P<0.01). PEFF also upregulated the expression of T-bet protein (P<0.05) but downregulated GATA3 protein (P<0.05) in nasal mucosa and spleen tissues. In conclusion, PEFF effectively reduces AR nasal symptoms and serum IgE levels in a mouse model and may act by correcting the imbalance between Th1 and Th2 responses.

circPARD3 drives malignant progression and chemoresistance of laryngeal squamous cell carcinoma by inhibiting autophagy through the PRKCI-Akt-mTOR pathway.

BACKGROUND: Laryngeal squamous cell carcinoma (LSCC) is the second most common malignant tumor in head and neck. Autophagy and circular RNAs (circRNAs) play critical roles in cancer progression and chemoresistance. However, the function and mechanism of circRNA in autophagy regulation of LSCC remain unclear. METHODS: The autophagy-suppressive circRNA circPARD3 was identified via RNA sequencing of 107 LSCC tissues and paired adjacent normal mucosal (ANM) tissues and high-content screening. RT-PCR, Sanger sequencing, qPCR and fluorescence in situ hybridization were performed to detect circPARD3 expression and subcellular localization. Biological functions of circPARD3 were assessed by proliferation, migration, invasion, autophagic flux, and chemoresistance assays using in vitro and in vivo models. The mechanism of circPARD3 was investigated by RNA immunoprecipitation, RNA pulldown, luciferase reporter assays, western blotting and immunohistochemical staining. RESULTS: Autophagy was inhibited in LSCC, and circPARD3 was upregulated in the LSCC tissues (n = 100, p < 0.001). High circPARD3 level was associated with advanced T stages (p < 0.05), N stages (p = 0.001), clinical stages (p < 0.001), poor differentiation degree (p = 0.025), and poor prognosis (p = 0.002) of LSCC patients (n = 100). Functionally, circPARD3 inhibited autophagy and promoted LSCC cell proliferation, migration, invasion and chemoresistance. We further revealed that activation of the PRKCI-Akt-mTOR pathway through sponging miR-145-5p was the main mechanism of circPARD3 inhibited autophagy, promoting LSCC progression and chemoresistance. CONCLUSION: Our study reveals that the novel autophagy-suppressive circPARD3 promotes LSCC progression and chemoresistance through the PRKCI-Akt-mTOR pathway, providing new insights into circRNA-mediated autophagy regulation and potential biomarker and target for LSCC treatment.

Targeting SKA3 suppresses the proliferation and chemoresistance of laryngeal squamous cell carcinoma via impairing PLK1-AKT axis-mediated glycolysis.

Spindle and kinetochore-associated complex subunit 3 (SKA3) is a well-known regulator of chromosome separation and cell division, which plays an important role in cell proliferation. However, the mechanism of SKA3 regulating tumor proliferation via reprogramming metabolism is unknown. Here, SKA3 is identified as an oncogene in laryngeal squamous cell carcinoma (LSCC), and high levels of SKA3 are closely associated with malignant progression and poor prognosis. In vitro and in vivo experiments demonstrate that SKA3 promotes LSCC cell proliferation and chemoresistance through a novel role of reprogramming glycolytic metabolism. Further studies reveal the downstream mechanisms of SKA3, which can bind and stabilize polo-like kinase 1 (PLK1) protein via suppressing ubiquitin-mediated degradation. The accumulation of PLK1 activates AKT and thus upregulates glycolytic enzymes HK2, PFKFB3, and PDK1, resulting in enhancement of glycolysis. Furthermore, our data reveal that phosphorylation at Thr360 of SKA3 is critical for its binding to PLK1 and the increase in glycolysis. Collectively, the novel oncogenic signal axis "SKA3-PLK1-AKT" plays a critical role in the glycolysis of LSCC. SKA3 may serve as a prognostic biomarker and therapeutic target, providing a potential strategy for proliferation inhibition and chemosensitization in tumors, especially for LSCC patients with PLK1 inhibitor resistance.

Crosstalk between RNA m6A Modification and Non-coding RNA Contributes to Cancer Growth and Progression.

N6-methyladenosine (m6A) is the most common RNA modification and has an important role in normal development and tumorigenesis. The abnormal expression of m6A regulators can lead to an imbalance in m6A levels in cancer cells, leading to the dysregulated expression of oncogenes and tumor suppressor genes that may contribute to cancer development, patient response to chemoradiotherapy, and clinical prognosis. Recent studies demonstrate that non-coding RNAs are involved in epigenetic modification of both DNA and RNA in tumor cells, and may also affect the development and progression of cancer by targeting m6A regulators. In this review, we describe the functional crosstalk between m6A and non-coding RNAs, particularly microRNA, long non-coding RNA, and circular RNA, and illustrate their roles in tumor regulation. Finally, we discuss the significance of non-coding RNA and m6A modification in the diagnosis, treatment, and prognosis of cancer patients, as well as potential future research directions.

Serum Exosomal miR-941 as a promising Oncogenic Biomarker for Laryngeal Squamous Cell Carcinoma.

At present, no blood-based biomarkers have been used in clinical practice for laryngeal squamous cell carcinoma (LSCC). Increasing evidence suggests that circulating exosomal microRNAs (miRNAs) may serve as potential diagnostic biomarkers for various cancers. This study aims to identify and evaluate serum exosomal miRNAs for LSCC diagnosis. The ExoQuick solution (EQ), which provides a high-yield and is a highly efficient exosome isolation method, was selected to isolate serum exosomes in the current study. In LSCC samples, exosome concentrations were higher than in healthy control (HC) samples. RNA-seq analysis identified a total of 1608 miRNAs, with 34 upregulated and 41 downregulated in LSCC samples relative to HC samples. Furthermore, qRT-PCR showed that miR-941 is significantly upregulated in LSCC serum exosomes, with this same trend seen in LSCC tissues and cells. Moreover, when examining miR-941 in cell lines, miR-941 overexpression promoted proliferation and invasion, while miR-941 knockdown inhibited cell proliferation and invasion. ROC curve analysis showed that miR-941 has an area under the curve (AUC) of 0.797 (95% CI = 0.676-0.918) for distinguishing LSCC patients from HCs. In conclusion, serum exosomal miR-941 may serve as a promising oncogenic biomarker for diagnosing LSCC, and has the potential as a therapeutic target.

Circular RNA circCORO1C promotes laryngeal squamous cell carcinoma progression by modulating the let-7c-5p/PBX3 axis.

BACKGROUND: Laryngeal squamous cell carcinoma (LSCC) is a common malignant tumor of the head and neck. LSCC patients have seriously impaired vocal, respiratory, and swallowing functions with poor prognosis. Circular RNA (circRNA) has attracted great attention in cancer research. However, the expression patterns and roles of circRNAs in LSCC remain largely unknown. METHODS: RNA sequencing was performed on 57 pairs of LSCC and matched adjacent normal mucosa tissues to construct circRNA, miRNA, and mRNA expression profiles. RT-PCR, qPCR, Sanger sequencing, and FISH were undertaken to study the expression, localization, and clinical significance of circCORO1C in LSCC tissues and cells. The functions of circCORO1C in LSCC were investigated by RNAi-mediated knockdown, proliferation analysis, EdU staining, colony formation assay, Transwell assay, and apoptosis analysis. The regulatory mechanisms among circCORO1C, let-7c-5p, and PBX3 were investigated by luciferase assay, RNA immunoprecipitation, western blotting, and immunohistochemistry. RESULTS: circCORO1C was highly expressed in LSCC tissues and cells, and this high expression was closely associated with the malignant progression and poor prognosis of LSCC. Knockdown of circCORO1C inhibited the proliferation, migration, invasion, and in vivo tumorigenesis of LSCC cells. Mechanistic studies revealed that circCORO1C competitively bound to let-7c-5p and prevented it from decreasing the level of PBX3, which promoted the epithelial-mesenchymal transition and finally facilitated the malignant progression of LSCC. CONCLUSIONS: circCORO1C has an oncogenic role in LSCC progression and may serve as a novel target for LSCC therapy. circCORO1C expression has the potential to serve as a novel diagnostic and prognostic biomarker for LSCC detection.

Non-coding RNAs in drug resistance of head and neck cancers: A review.

Head and neck cancer (HNC), which includes epithelial malignancies of the upper aerodigestive tract (oral cavity, oropharynx, pharynx, hypopharynx, larynx, and thyroid), are slowly but consistently increasing, while the overall survival rate remains unsatisfactory. Because of the multifunctional anatomical intricacies of the head and neck, disease progression and therapy-related side effects often severely affect the patient's appearance and self-image, as well as their ability to breathe, speak, and swallow. Patients with HNC require a multidisciplinary approach involving surgery, radiation therapy, and chemotherapeutics. Chemotherapy is an important part of the comprehensive treatment of tumors, especially advanced HNC, but drug resistance is the main cause of poor clinical efficacy. The most important determinant of this phenomenon is still largely unknown. Recent studies have shown that non-coding RNAs have a crucial role in HNC drug resistance. In addition, they can serve as biomarkers in the diagnosis, treatment, and prognosis of HNCs. In this review, we summarize the relationship between non-coding RNAs and drug resistance of HNC, and discuss their potential clinical application in overcoming HNC chemoresistance.

Mass Spectrometric Analysis Identifies AIMP1 and LTA4H as FSCN1-Binding Proteins in Laryngeal Squamous Cell Carcinoma.

Dysregulation of fascin actin-bundling protein 1 (FSCN1) enhances cell proliferation, invasion, and motility in laryngeal squamous cell carcinoma (LSCC), while the mechanism remains unclear. Here, co-immunoprecipitation and mass spectrometry is utilized to identify potential FSCN1-binding proteins. Functional annotation of FSCN1-binding proteins are performed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis. Furthermore, the protein-protein interaction network of FSNC1-binding proteins is constructed and the interactions between FSCN1 and novel identified interacting proteins AIMP1 and LTA4H are validated. Moreover, the expression and functional role of AIMP1 and LTA4H in LSCC are investigated. A total of 123 proteins are identified as potential FSCN1-binding proteins, and functional annotation shows that FSCN1-binding proteins are significantly enriched in carcinogenic processes, such as filopodium assembly-regulation and GTPase activity. Co-IP/western blotting and immunofluorescence confirm that AIMP1 and LTA4H bind and colocalize with FSCN1. Furthermore, both AIMP1 and LTA4H are upregulated in LSCC tissues, and knockdown of AIMP1 or LTA4H inhibits LSCC cell proliferation, migration, and invasion. Collectively, the identification of FSCN1-binding partners enhances understanding of the mechanism of FSCN1-mediated malignant phenotypes, and these findings indicate that FSCN1 binds to AIMP1 and LTA4H might promote the progression of LSCC.