PURPOSE:Invasive fungal infections are a serious threat to immunocompromised individuals, with laryngeal involvement being rare and often presenting with atypical symptoms that complicate early diagnosis. METHODS:The authors report a case of chronic invasive fungal laryngeal cartilage necrosis, initially manifesting as bilateral vocal cord fixation. RESULTS:Pathology suggested Mucorales infection. Postoperative recovery included resolution of both laryngeal and pulmonary issues after a total laryngectomy. There has been no recurrence at follow-up visits. CONCLUSION:Early diagnosis, aggressive surgical debridement, and full-course antifungal treatment are essential for improving outcomes in extrapulmonary fungal infections.

OBJECTIVE:To investigate the application value, technical advantages, clinical efficacy, educational impact, and challenges in promotion of the Da Vinci robotic surgical system (Transoral Robotic Surgery, TORS) in complex head and neck surgeries, providing a reference for the advancement of precise and intelligent surgery in this field. METHODS:The technical principles and evolution of the Da Vinci system were analyzed. Its clinical application data in laryngeal, oropharyngeal, obstructive sleep apnea (OSA), nasal cavity, and thyroid surgeries were reviewed. The supporting role of digital technologies (AI, 3D visualization, VR, 3D printing) was assessed. Challenges related to cost and training requirements were summarized. RESULTS:Leveraging advantages such as instrument flexibility, high-definition 3D visualization, tremor filtration, and precise manipulation, the Da Vinci system significantly enhanced outcomes in head and neck surgery: precise resection of laryngeal cancer reduced operative risks; efficient treatment of early-stage oropharyngeal squamous cell carcinoma (OPSCC) was achieved with fewer complications; favorable long-term survival rates were observed for OPSCC; OSA symptoms were effectively improved; and it demonstrated both minimally invasive benefits and therapeutic efficacy in recurrent nasal cavity cancers and thyroid surgeries. Digital technologies enhanced surgical precision and medical training efficiency. However, high unit costs and stringent training requirements limit its adoption in small and medium-sized hospitals. CONCLUSION:The Da Vinci system, integrated with digital technologies, significantly improves the safety, precision, and patient prognosis in head and neck surgery, while elevating medical education standards. High costs and intensive training needs are issues for why it is not widely used. Future tasks should emphasize cost-cutting to enhance patient care access and improve quality across the medical spectrum.

BACKGROUND:Based on bioinformatics research of NUDT21 in pan-cancer, we aimed to clarify the mechanism of NUDT21 in HHNC by experiment. METHODS:The correlation between differential expression of NUDT21 in pan-cancer and survival prognosis, genomic instability, tumor stemness, DNA repair, RNA methylation and with immune microenvironment were analyzed by the application of different pan-cancer analysis web databases. In addition, immunohistochemistry staining and genetic detection of NUDT21 in HHNCC tumor tissues by immunohistochemistry and qRT-PCR. Then, through in vitro cell experiments, NUDT21 was knocked down by lentivirus to detect the proliferation, cycle, apoptosis of FaDu and CNE-2Z cells, and finally by PathScan intracellular signaling array reagent to detect the apoptotic protein content. RESULTS:Based on the pan-cancer analysis, we found that elevated expression of NUDT21 in most cancers was significantly correlated with TMB, MSI, neoantigens and chromosomal ploidy, and in epigenetics, elevated NUDT21 expression was strongly associated with genomic stability, mismatch repair genes, tumor stemness, and RNA methylation. Based on immunosuppressive score, we found that NUDT21 plays an essential role in the immunosuppressive environment by suppressing immune checkpointing effect in most cancers. In addition, using HHNSCC as a study target, PCR and pathological detection of NUDT21 in tumor tissues was significantly increased than that in paracancerous normal tissues. In vitro cellular assays, silencing NUDT21 inhibited proliferation and promoted apoptosis in FaDu and CNE-2Z cells, and blocked the cell cycle in the G2/M phase. Therefore, the experiments confirmed that NUDT21 promotes the proliferation of FaDu by suppressing the expression of apoptotic.

(NK) cells are at the first line of defence against tumours, but their anti‐tumour mechanisms are not fully understood. We aimed to investigate the mechanism by which NK cells can mediate immunotherapy against head and neck squamous cell carcinoma (HNSCC). We collected fifty‐two pairs of HNSCC tissues and corresponding adjacent normal tissues; analysis by RT‐qPCR showed underexpression of CXCL14 in HNSCC tissues. Primary NK cells were then isolated from the peripheral blood of HNSCC patients and healthy donors. CXCL14 was found to be consistently under‐expressed in the primary NK cells from the HNSCC patients. However, CXCL14 expression was increased in IL2‐activated primary NK cells and NK‐92 cells. We next evaluated NK cell migration, IFN‐γ and TNF‐α expression, cytotoxicity and infiltration in response to CXCL14 overexpression or knockdown using gain‐ and loss‐of‐function approach. The results exhibited that CXCL14 overexpression promoted NK cell migration, cytotoxicity and infiltration. Subsequent in vivo experiments revealed that CXCL14 suppressed the growth of HNSCC cells via activation of NK cells. ChIP was applied to study the enrichment of H3K27ac, p300, H3K4me1 and CDX2 in the enhancer region of CXCL14, which showed that CDX2/p300 activated the enhancer of CXCL14 to up‐regulate its expression. Rescue experiments demonstrated that CDX2 stimulated NK cell migration, cytotoxicity and infiltration through up‐regulating CXCL14. In vivo data further revealed that CDX2 suppressed tumorigenicity of HNSCC cells through enhancement of CXCL14. To conclude, CDX2 promotes CXCL14 expression by activating its enhancer, which promotes NK cell–mediated immunotherapy against HNSCC.

Dihydrotanshinone (DIH) is an extract of Salvia miltiorrhiza Bunge. It has been reported that DIH could regulate NF-κB signaling pathway. The aim of this study was to investigate whether DIH could protect mice from lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. In this study, sixty mice were randomly divided into five groups, one group as blank control group, the second group as LPS control group, and the last three groups were pre-injected with different doses of DIH and then inhaled LPS for experimental comparison. After 12 h of LPS treatment, the wet-dry ratio, histopathlogical changes, and myeloperoxidase (MPO) activity of lungs were measured. In addition, ELISA kits were used to measure the levels of TNF-α and IL-1β inflammatory cytokines in bronchoalveolar lavage fluids (BALF), and western blot analysis was used to measure the activity of NF-κB signaling pathway. The results demonstrated that DIH could effectively reduce pulmonary edema, MPO activity, and improve the lung histopathlogical changes. Furthermore, DIH suppressed the levels of inflammatory cytokines in BALF, such as TNF-α and IL-1β. In addition, DIH could also downregulate the activity of NF-κB signaling pathway. We also found that DIH dose-dependently increased the expression of LXRα. In addition, DIH could inhibit LPS-induced IL-8 production and NF-κB activation in A549 cells. And the inhibitory effects were reversed by LXRα inhibitor geranylgeranyl pyrophosphate (GGPP). Therefore, we speculate that DIH regulates LPS-induced ALI in mice by increasing LXRα expression, which subsequently inhibiting NF-κB signaling pathway.

MicroRNA (miR)-410 plays a potential role in the pathogenesis of atherosclerosis. The current study mainly focuses on the underlying mechanism of miR-410/histone deacetylase 1 (HDAC1)/KLF5/nuclear factor κB (NF-κB) inhibitor α (IKBα)/NF-κB axis in atherosclerosis. miR-410 expression was determined using quantitative real-time PCR in both mouse models of atherosclerosis and human umbilical endothelial cells (HUVECs) treated with oxidized low-density lipoprotein (ox-LDL). The study subsequently predicted regulators associated with miR-410 through bioinformatics, and their binding relation was further verified through dual luciferase reporter gene and RNA immunoprecipitation (RIP) assays, and how HDAC1 regulated KLF5 was tested through coimmunoprecipitation (coIP). In HUVECs, miR-410 and HDAC1 mRNA expression; HDAC1, KLF5, IKBα, p65, p-p65, VCAM-1, ICAM-1, and MCP-1 protein expression; and inflammatory cytokine expressions were detected using quantitative real-time PCR, western blot, and ELISA. The present study further tested cell functions by Cell Counting Kit-8 (CCK-8), flow cytometry, and the colony-formation assay. It was revealed that miR-410 could target HDAC1, whereas HDAC1 could target transcription factor KLF5, increasing IKBα expression, thus suppressing NF-κB in atherosclerosis. Furthermore, silencing miR-410 or overexpressing HDAC1 increased cell viability and suppressed apoptosis and an inflammatory reaction in HUVECs in atherosclerosis. Blocking miR-410 promotes HDAC1 expression and increases IKBα levels through KLF5 to suppress NF-κB, thus preventing development of atherosclerosis.

Vanillin, the main constituents of vanillin beans, has been reported to exhibit anti-inflammatory effects. However, the effects of vanillin on the cadmium-induced lung injury are still unclear. Therefore, we assay whether vanillin has potential preventive activity on cadmium-induced lung injury in mice. Mice were given vanillin (5, 10, 20 mg/kg) and treated with cadmium for 7 days. The detection data of vanillin on lung tissue changes were analyzed after the cadmium treatment. The results displayed that vanillin obviously decreased the lung histological alterations and myeloperoxidase (MPO) activity. Vanillin also suppressed the levels of TNF-α, IL-1β, and IL-6 in BALF. Furthermore, vanillin prevented cadmium-induced NF-κB activation and upregulation the expression of tight junction protein ZO-1 and occludin. In addition, vanillin significantly increased the expression of aryl hydrocarbon receptor (AhR), and inhibition of AhR by its agonist could reverse the protective effects of vanillin on cadmium-induced lung injury. To sum up, vanillin could be a potential drug for the treatment of cadmium-induced lung injury.

下咽癌是上消化呼吸道恶性程度最高的肿瘤之一.目前对于下咽癌的治疗,首选治疗方法是以手术治疗为主的综合治疗.基于肿瘤病灶的异质性,我们选择不同治疗策略.肿瘤原发灶的位置决定手术入路;病灶不同的临床特点,如小病灶大转移、浅表扩展癌、多点多灶癌等,其治疗策略具有差异性;手术切缘的范围一直是探讨和争论的热点.本文针对于以上问题,进行经验分享及相关文献总结.针对不同类型的下咽癌,为其制定最佳的个性化的治疗策略,以改善预后,提高生存率.

Retraction: "microRNA-539 functions as a tumor suppressor in papillary thyroid carcinoma via the transforming growth factor beta 1/Smads signaling pathway by targeting secretory leukocyte protease inhibitor," by Cheng-Bi Xu, Xue-Shi-Bo-Jie Liu, Jin-Qiu Li, Xue Zhao, Ding Xin, Dan Yu, J Cell Biochem. 2019; 10830-10846: The above article, published online on 31 January 2019 in Wiley Online Library (), has been retracted by agreement between the journal's Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. As several flaws and inconsistencies between results presented and experimental methods described were found, the editors consider the conclusions of this article to be invalid.

Background This study seeks to assess interleukin-37 (IL-37) serum level in acute ischemic stroke and the value of predicting 3-month stroke recurrence and functional outcome in acute ischemic stroke. Methods From January 1, 2018, to June 30, 2019, all consecutive first-ever acute ischemic stroke patients from our hospital, China, were included. Serum samples, clinical information, and stroke severity (defined by the National Institute of Health stroke scale (NIHSS) score) were collected at baseline. Serum IL-37 level was measured by the enzyme-linked immunosorbent assay (ELISA) method. Functional impairment (defined by the modified Rankin scale (mRS)) and recurrent stroke were assessed 3 months after admission. The relation of IL-37 with either clinical severity at baseline, unfavorable functional outcome, or stroke recurrence at follow-up was evaluated by logistic regression analysis, and the results were presented as odds ratios (OR) with 95% confidence intervals (CI). Results Three hundred and ten stroke patients were included. The median IL-37 serum level in those patients was 344.1 pg/ml (interquartile range (IQR), 284.4-405.3 vs. control cases: 122.3 pg/ml (IQR, 104.4-1444.0); P < 0.001). At 3 months, a total of 36 (11.6%) patients had a stroke recurrence. IL-37 serum levels in those patients were higher than in those patients without stroke recurrence (417.0 pg/ml (IQR, 359.3-436.1) vs. 333.3 pg/ml (279.0-391.0)). In a logistic model adjusted for other factors, IL-37 in the highest quartile (>405.3 pg/ml) was still associated with recurrent stroke (OR = 3.32; 95%CI = 2.03–6.13; P < 0.001). IL-37 could promote the NIHSS score (area under the curve (AUC) of the IL-37/NIHSS, 0.75; 95% CI, 0.67–0.83; P < 0.001), corresponding to a difference of 0.085 (0.005). Serum IL-37 increases in patients with poor outcome, and an IL-37 in the highest quartile is related to poor outcome (OR = 4.85; 95%CI = 3.11 − 8.22; P < 0.001). Conclusion Serum IL-37 increased in patients after ischemic stroke and was associated with stroke recurrence events and poor stroke outcomes. Large randomized controlled trials should be carried out to confirm whether IL-37 lowering treatment improves stroke prognosis.

Purpose The etiology of nasopharyngeal carcinoma (NPC) is multifactorial, complex and not fully characterized yet. MicroRNAs (miRNAs or miRs) have been found to contribute to the development and progression of NPC. Here, we aimed to investigate the putative role of miR-129-5p in NPC lymphangiogenesis and lymph node metastasis (LNM), including the involvement of its target gene ZIC2 and the Hedgehog signaling pathway. Methods The expression of miR-129-5p and ZIC2 in primary NPC tissues was assessed using RT-qPCR and Western blot analyses, followed by LNM and lymph vessel density (LVD) correlation analyses. A direct interaction between miR-129-5p and ZIC2 was verified using a dual-luciferase reporter assay. Gain- and loss-of-function experiments were conducted to investigate the effects of miR-129-5p and ZIC2 expression on NPC cell invasion, migration and proliferation in vitro, as well as on LDV and LNM in nude mice in vivo. Additionally, RT-qPCR and Western blot analyses were performed to determine the expression levels of Hedgehog signaling pathway-related factors. Results We found that ZIC2 was highly expressed, and miR-129-5p was lowly expressed, in primary NPC tissues. In addition, we found that miR-129-5p can directly bind to and reduce ZIC2 expression. LVD was found to be negatively correlated with miR-129-5p and to be positively correlated with ZIC2 expression. Concomitantly, we found that miR-129-5p abrogated activation of the Hedgehog signaling pathway via ZIC2 targeting, leading to suppression of NPC cell invasion, migration and proliferation in vitro as well as suppression of LNM and LVD in vivo. Conclusions From our data we conclude that miR-129-5p, by decreasing ZIC2 expression, may inhibit NPC lymphangiogenesis and LNM through suppression of the Hedgehog signaling pathway.

Nasopharyngeal carcinoma ( NPC ) is a common cancer found in the nasopharynx with high metastatic and invasive nature. Increasing evidences have identified the critical role of gene therapy in NPC treatment. Hence, this study was designed to identify specific gene markers that affected NPC progression through gene expression profile analysis. NPC ‐related gene expression data set gene set enrichment ( GSE )53819 were retrieved and analyzed to screen out differentially expressed genes ( DEG s), followed by determination of their expression in noncancerous tissues and NPC specimens. Next, weighted gene co‐expression network analysis ( WGCNA ) was conducted on DEG s to obtain tumor‐associated gene modules. Genes in those modules were intersected with DEG s for gene ontology and Kyoto Encyclopedia of Genes and Genomes functional enrichment analysis. Then protein‐protein interaction network of tumor‐associated genes was constructed to select genes most closely linked to NPC . Afterward, expression of chromosome 9 open reading frame 24 (c9orf24), primary ciliary dyskinesia protein 1 ( PCDP 1), and leucine‐rich repeat‐containing protein 46 ( LRRC 46) was detected in GSE 53819 and further verified in GSE 12452 and GSE 64634. Differential analysis on GSE 53819 found that 2,173 genes were aberrantly expressed in NPC , among which 917 genes are upregulated and 1,256 genes are downregulated. WGCNA showed that genes were enriched in 17 modules and 727 genes exhibited ectopic expression in NPC and enriched in cytokine‐cytokine receptor interaction, cytochrome P450, and chemical carcinogenesis signaling pathways, among which c9orf24, PCDP 1, and LRRC 46 were poorly expressed in NPC . Therefore, c9orf24, PCDP 1, and LRRC 46 might serve as prominent diagnostic markers for NPC , which presents new insights for NPC therapy.

Aberrant expression of LINC00520 has been identified in head and neck squamous carcinoma (HNSCC). However, its function in the radiosensitivity of HNSCC remain unclear. Herein, we aimed to define the role LINC00520 in the radiosensitivity of HNSCC and identify the underlying mechanism. Tumour tissues and adjacent normal tissue were collected from HNSCC patients. Differentially expressed genes (DEGs) in HNSCC tumour were obtained from the cancer genome atlas (TCGA) database. Interactions between LINC00520 and miR-195, homeobox A10 (HOXA10) and miR-195 were evaluated by dual-luciferase reporter gene assay, RNA Immunoprecipitation (RIP), and RNA pull-down assay. The effects of LINC00520/miR-195/HOXA10 on radiosensitivity of HNSCC were analysed in the evaluation of radiotherapy outcome. Cell proliferation, invasion, migration, and apoptosis of HNSCC cells were accessedviagain- and loss-of-function approaches. Tumour xenograft in nude mice was conducted in order to confirm the resultsin vivo. LINC00520 was upregulated while miR-195 was downregulated in HNSCC cells and tissues. Silencing LINC00520 or overexpressing miR-195 promoted radiosensitivity and inhibited cell proliferation, invasion, migration, and apoptosis in HNSCC. Moreover, thesein vitrofindings were reproducedin vivoin human HNSCC xenograft in nude mice. LINC00520/miR-195/HOXA10 is involved in the radiosensitivity mediation, providing potential therapeutic target for HNSCC treatment.

医学科技进步日新月异，对于具有敏锐创新思维的多学科交叉创新型人才的需要迫在眉睫。基于已广泛应用于临床的多学科诊疗模式，我们将多学科诊疗引入教学系统，构建了一个培养多学科交叉创新型人才的新的教学体系，从单一特定学科培养模式向多学科交叉综合培养模式转变，提高了学生自主创新能力及思维，增强了学生的团结协作精神及医学人文素养，为我国医疗事业储备高层次复合型人才。

癌肉瘤是一种包含有癌和肉瘤两种恶性成分的肿瘤,其恶性程度高,发病率低,发生于腮腺的癌肉瘤罕见,难以与其他腮腺肿瘤相鉴别,确诊必须靠术后病理.本文报道1例我院收治的腮腺癌肉瘤,并结合文献复习,对腮腺癌肉瘤的鉴别诊断及治疗进行讨论. 1临床资料 患者男,69岁,因发现左侧腮腺区肿物40年,迅速增大4个月而入院,查体:左侧耳根部可触及一类圆形肿块,大小约为4 cm×5 cm,包块表面光滑,皮肤无红肿破溃,质地硬,活动度差,边界尚清,轻压痛,露齿时口角下坠,微笑时面部歪斜,鼓腮时漏气.

Neurodegeneration in Alzheimer’s disease (AD) results in microglial activation, which may participate in the inflammatory cascade accelerating tissue damage. In this study, we sought to characterize the alleviatory role of microRNA-711 (miR-711) encapsulated in microglia-derived extracellular vesicles (EVs) in a model of AD. Ultracentrifugation was employed to extract EVs from microglia (BV2 cells), which were identified using Western blot analysis of the EVs marker proteins Alix and CD63. A repetitive mild traumatic brain injury (rmTBI) mouse model was induced by controlled cortical impact. After overexpressing miR-711 or 1,4,5-trisphosphate 3-kinase B (Itpkb) in BV2 cells, we evaluated the inflammation in BV2 cells and the ratio of microglia M2/M1. Further, we injected BV2 cell-secreted EVs with overexpressed miR-711 or Itpkb into rmTBI mice through a tail vein to investigate the inflammation markers in mouse serum and, the M2/M1 phenotype ratio of microglia in brain tissues, and to evaluate neurological deficit and cognitive function. The EVs obtained by ultracentrifugation were verified by the presence of Alix and CD63 expression. Mechanistic studies suggested that miR-711 targeted and inhibited Itpkb, thereby repressing Tau phosphorylation and increasing the ratio of M2/M1. Furthermore, miR-711-containing EVs reduced the score of neurological deficits and improved cognitive function in rmTBI mice. The administration of microglia-derived EVs loaded with miR-711, which mediated the hyperphosphorylation of Tau protein in the Itpkb pathway, effectively alleviated neurodegenerative changes and cognitive dysfunction in AD.

Papillary thyroid carcinoma (PTC) is the most common type of thyroid malignancy, with growing incidence every year. microRNAs (miRs) are known to regulate the physiological and pathological processes of cancers, such as proliferation, migration, invasion, survival, and epithelial-mesenchymal transition (EMT). Herein, this study aimed to investigate the effect of miR-539 on cell proliferation, apoptosis, and EMT by targeting secretory leukocyte protease inhibitor (SLPI) via the transforming growth factor β1 (TGF-β1)/Smads signaling pathway in PTC. First, PTC-related differentially expressed genes and regulatory miR were screened using bioinformatics analysis, dual luciferase reporter gene assay, and ribonucleoprotein immunoprecipitation, which identified the SLPI gene and the regulatory miR-539 for this study. We identified SLPI as a highly expressed gene in PTC tissues, and SLPI was targeted and negatively regulated by miR-539. Then, we introduced a series of miR-539 mimics, miR-539 inhibitors, and small interfering RNA against SLPI plasmids into CGTHW-3 cells to examine the effects of miR-539 and SLPI on the expression of TGF-β1/Smads signaling pathway-, EMT-, and apoptosis-related factors, as well as cell proliferation, migration, invasion, and apoptosis. The obtained results indicated that CGTHW-3 cells treated with silenced SLPI or overexpressed miR-539 suppressed the cell proliferation, migration, invasion abilities, and resistance to apoptosis of PTC cells, corresponding to increased expression of Bcl-2-associated X protein, TGF-β1, Sekelsky mothers against dpp 4, and epithelial cadherin, and decreased B cell lymphoma 2, Vimentin, and N-cadherin. Altogether, we concluded that overexpressed miR-539 could inhibit the PTC cell proliferation and promote apoptosis and EMT by targeting SPLI via activation of the TGF-β1/Smads signaling pathway.

Background: In this study, we examined whether RORA (retinoic acid receptor-related orphan receptor alpha) was capable of alleviating the progression of allergic rhinitis (AR). Methods: In order to elucidate the possible effects of RORA and the regulatory mechanism between RORA and the Wnt/β-catenin signaling pathway, mouse AR models were established and treated with RORA vector, siRNA against RORA, or the Wnt/β-catenin pathway inhibitor WIF-1. Subsequently, the serum levels of inflammatory cytokines (IgE, INF-γ, IL-1β, IL-4, and IL-17), red blood cell (RBC) immune adhesion function, the levels of RORA, β-catenin, and GSK3β, as well as the extent of β-catenin and GSK-3β phosphorylation were evaluated and measured. Results: The OVA-induced AR mouse model exhibited obvious nasal mucosal injury and inflammatory cell infiltration. RORA overexpression or the inactivation of the Wnt/β-catenin signaling pathway was uncovered as a way to ameliorate nasal mucosal injury and eosinophil infiltration of the OVA-induced AR mouse model. On the other hand, it reduced the number of eosinophils and mast cells, which also resulted in downregulated expression of IgE, INF-γ, IL-1β, IL-4, IL-17, β-catenin, and GSK-3β. Moreover, this led to a decreased extent of β-catenin and GSK-3β phosphorylation, while the rates of C3b receptor rosette and Ic rosette were elevated. Conclusion: Taken together, the key findings provided evidence suggesting that the elevated RORA could potentially alleviate nasal mucosal injury and simultaneously enhance RBC immune adhesion function through the inhibition of the Wnt/β-catenin signaling pathway activation in an OVA-induced AR mouse model. This emphasizes a novel therapeutic target for the treatment of AR.

Aim: Head and neck squamous cell carcinoma (HNSCC) is one of the most prevalent types of cancer worldwide with unfavorable patient outcomes and relatively low survival rates. Long non-coding RNAs (lncRNAs) have been demonstrated to participate in the progression of HNSCC. The present study aimed to investigate the functional mechanism of lncRNA LINC00460 in HNSCC by mediating microRNA-206 (miR-206)/stanniocalcin-2 (STC2) axis. Methods: The interactions among miR-206, LINC00460 and STC2 were identified, and the expression of LINC00460, miR-206 and STC2 in tissues and cells was determined. Gain- and loss-of function experiments were conducted to analyze effects of LINC00460, miR-206 and STC2 on the expression of apoptosis-related proteins, autophagy-related proteins, and the extents of AKT, ERK phosphorylation. Cell cycle distribution, apoptosis and the production of autophagosomes after transfection were evaluated to further explore the role of LINC00460/ miR-206/STC2 axis in HNSCC. Results: LINC00460 and STC2 were highly expressed while miR-206 was poorly expressed in HNSCC. Besides, miR-206 was found to bind to both LINC00460 and STC2. After the transfection of HNSCC cells with miR-206 mimic or si-LINC00460, the expression of STC2, AKT, ERK, as well as the extent of AKT, ERK phosphorylation all decreased, which facilitated the apoptosis and autophagy of HNSCC cells. Conclusion: Collectively, the apoptosis and autophagy of HNSCC can be facilitated by downregulating LINC00460, which highlights a novel target in the treatment of HNSCC.