Nasopharyngeal carcinoma (NPC) is characterized by high metastatic potential and therapeutic resistance, necessitating the development of novel and safe therapeutic strategies. Hyperactivation of the PI3K/AKT signaling pathway, often driven by the oncogenic microRNA-21 (miR-21) and the subsequent suppression of PTEN, plays a key role in NPC progression. Chelerythrine (CHE), a natural plant-derived alkaloid, exhibits potent anti-tumor activities; however, its precise regulatory mechanisms and translational potential in NPC remain elusive. Network pharmacology was employed to predict the core downstream cascades of CHE against NPC. In vitro, CCK-8, real-time cellular analysis (RTCA), flow cytometry, wound healing, and Transwell assays were utilized to evaluate the specific cytotoxicity and anti-malignant effects of CHE in normal nasopharyngeal epithelial cells (NP69) and NPC cells (5–8 F and 6-10B). RT-qPCR was used to quantify the expression of primary (pri-miR-21), precursor (pre-miR-21), and mature miR-21. In vivo, a BALB/c nude mouse xenograft model was established to systematically assess the tumor-suppressive efficacy and macroscopic/histological biosafety of CHE. Furthermore, definitive rescue experiments were conducted using a specific PI3K activator and lentivirus-mediated miR-21 modification cell lines. Network pharmacology highlighted the PI3K/AKT pathway as the key effector cascade of CHE. Functionally, CHE exhibited a highly favorable safety profile in NP69 cells and in vivo major organs, while significantly inhibiting NPC cell proliferation, migration, and invasion, and inducing apoptosis. Mechanistically, CHE synchronously suppressed the expression of pri-miR-21 and pre-miR-21, indicating a transcriptional downregulation of miR-21. This upstream suppression led to the restoration of the tumor suppressor PTEN, subsequent inactivation of the PI3K/AKT pathway, and reversal of the epithelial-mesenchymal transition (EMT) phenotype. Importantly, co-treatment with a PI3K activator or lentiviral overexpression of miR-21 significantly counteracted the tumor-suppressive effects of CHE, whereas miR-21 knockdown synergistically potentiated its efficacy. Collectively, our findings indicate that CHE is a safe and effective therapeutic candidate for NPC. It exerts its anti-tumor and anti-metastatic effects by transcriptionally downregulating miR-21, thereby relieving PTEN suppression and systematically inactivating the PI3K/AKT signaling axis.

Objectives Nasopharyngeal carcinoma (NPC) is an aggressive head and neck malignancy in which post-treatment recurrence and distant metastasis remain major contributors to poor clinical outcomes. Although microRNAs are important post-transcriptional regulators of tumor progression, the role of miR-320d in NPC remains incompletely understood. This study evaluated the biological role of miR-320d and explored whether it is involved in regulating neutrophil extracellular trap (NET) formation through the nuclear factor kappa-B (NF-u03BAB)/interleukin-8 (IL-8) signaling axis. Methods miR-320d was overexpressed in NPC cell lines S18 and 5-8F, and cell viability, migration, and invasion were evaluated. Integrated transcriptomic and proteomic analyses were performed to identify miR-320d-regulated genes, proteins, and pathways. Western blotting, immunohistochemistry, and immunofluorescence analyses were used to validate NET-associated proteins, including glycoprotein Ib platelet subunit alpha (GP1BA), histone deacetylase 10 (HDAC10), and fibrinogen gamma chain (FGG), as well as the expression of NET formation markers, including peptidyl arginine deiminase 4 (PADI4), myeloperoxidase (MPO), and neutrophil elastase (NE); and key components of the NF-u03BAB/IL-8 axis. Results miR-320d overexpression significantly inhibited the viability, migration, and invasion of both S18 and 5-8F cells. Multi-omics analyses indicated that miR-320d-regulated molecules were mainly enriched in NET-related pathways. Consistently, miR-320d reduced the expression of GP1BA, HDAC10, FGG, PADI4, MPO, and NE. Mechanistically, miR-320d suppressed NF-u03BAB signaling, as shown by decreased phosphorylated NF-u03BAB (p-NF-u03BAB) and total NF-u03BAB levels, and reduced IL-8 secretion in NPC cells. Conclusion miR-320d may suppress NPC progression, at least in part, by attenuating NF-u03BAB/IL-8-associated NET formation. These findings suggest that the miR-320d/NF-u03BAB/IL-8/NET regulatory axis may participate in NPC progression and may warrant further translational investigation.

METHODS:Molecular docking was employed to analyze the binding affinity between the active components of YQJDF and AKT1. MTT assay, real-time cell analysis (RTCA), wound healing assay and Matrigel invasion chamber assay were used to evaluate the effect of YQJDF extract on proliferation, migration and invasion abilities of human NPC cell lines 5-8F and 6-10B, and the changes in cellular protein expression levels were detected using Western blotting. In a BALB/c nude mouse model bearing NPC cell xenografts, tumor growth were observed following treatment with daily gavage with normal saline or YQJDF extract (15.357 g/kg) for 18 consecutive days or with intraperitoneal injections of 5-Fu every other day. The changes in the expressions of AKT1/GLUT1 signaling axis proteins in the xenografts were examined using Western blotting. RESULTS:In the NPC cell lines, treatment with YQJDF extract significantly inhibited cell proliferation, migration, and invasion, and downregulated the expressions of p-AKT, GLUT1, XIAP, N-cadherin, and vimentin. The application of GLUT1 or AKT1 activators partially reversed the inhibitory effects of YQJDF on the NPC cells. In the tumor-bearing mouse models, treatment with YQJDF extract obviously suppressed tumor growth and down-regulated the expression of AKT, p-AKT and GLUT1 in the tumor tissues. CONCLUSIONS:YQJDF inhibits proliferation, invasion, and migration of NPC cells by inhibiting the AKT1/GLUT1 signaling pathway.

The intratumoral microbiome, comprising diverse bacteria, fungi, and viruses residing within tumor tissues, is increasingly recognized as a multidimensional oncogenic modulator, acting akin to a “microbial conductor” orchestrating key cancer hallmarks. Its compositon exhibits substantial heterogeneity across individuals and is closely associated with the host immunity, the tumor microenvironment (TME), and therapeutic efficacy. Specific microbial species can “conduct” pro-tumorigenic processes by producing carcinogenic metabolites, dysregulating inflammatory signaling, or facilitating immune evasion. Conversely, other microorganisms may exert anti-tumorigenic effects by stimulating anti-tumor immunity or directly inhibiting cancer cell proliferation. Furthermore, the intratumoral microbiome can influence therapeutic outcomes by modulating the metabolism of chemotherapeutic agents or altering the efficacy of immunotherapies. Therefore, a deeper understanding of the intratumoral microbiome and its complex interplay with tumors holds immense potential to unravel fundamental mechanisms of cancer development and progression, while simultaneously revealing novel avenues for precision oncology strategies. This review outlines the biological roles of the microbiota in modulating the hallmarks of cancer hallmarks, summarizes current knowledge on its multidimensional interactions driving tumor progression, and discusses the translational potential of targeting or leveraging the intratumoral microbiome based on recent advancements. Future research integrating multi-omics profiling, spatial technologies, and functional validation will be essential for resolving methodological limitations and accelerating the clinical translation of microbiome-based interventions.

Uterine leiomyosarcoma (ULMS) is a rare yet aggressive uterine malignancy with high recurrence and poor survival, prompting an urgent search for better treatments. We investigated whether atorvastatin, an HMG-CoA reductase inhibitor, could suppress ULMS growth by targeting mevalonate pathway-dependent prenylation. Human ULMS cell lines received atorvastatin ± isoprenoids to assess proliferation, cell-cycle distribution, and smooth muscle contractility, whereas proteomic profiling (LC-MS/MS) and in vivo xenografts were used to evaluate molecular pathways and antitumor efficacy. Atorvastatin inhibited ULMS proliferation in a dose-dependent manner, induced G₀/G₁ cell-cycle arrest, and diminished the contractile phenotype. Geranylgeranyl pyrophosphate rescued these effects, implicating geranylgeranylation as the key dependency, and Rap1A/Rap1B Western blotting confirmed functional GGPP depletion. In xenografts, atorvastatin suppressed ULMS tumor growth by ~50% with minimal toxicity, as evidenced by normal serum ALT and creatinine levels and preserved organ histology. These findings identify protein geranylgeranylation as a novel therapeutic vulnerability in ULMS and support statin repurposing as a promising treatment strategy.

Objectives: Nasopharyngeal carcinoma (NPC) is an aggressive head and neck malignancy in which post-treatment recurrence and distant metastasis remain major contributors to poor clinical outcomes. Although microRNAs are important post-transcriptional regulators of tumor progression, the role of miR-320d in NPC remains incompletely understood. This study evaluated the biological role of miR-320d and explored whether it is involved in regulating neutrophil extracellular trap (NET) formation through the nuclear factor kappa-B (NF-κB)/interleukin-8 (IL-8) signaling axis. Methods: miR-320d was overexpressed in NPC cell lines S18 and 5-8F, and cell viability, migration, and invasion were evaluated. Integrated transcriptomic and proteomic analyses were performed to identify miR-320d-regulated genes, proteins, and pathways. Western blotting, immunohistochemistry, and immunofluorescence analyses were used to validate NET-associated proteins, including glycoprotein Ib platelet subunit alpha (GP1BA), histone deacetylase 10 (HDAC10), and fibrinogen gamma chain (FGG), as well as the expression of NET formation markers, including peptidyl arginine deiminase 4 (PADI4), myeloperoxidase (MPO), and neutrophil elastase (NE); and key components of the NF-κB/IL-8 axis. Results: miR-320d overexpression significantly inhibited the viability, migration, and invasion of both S18 and 5-8F cells. Multi-omics analyses indicated that miR-320d-regulated molecules were mainly enriched in NET-related pathways. Consistently, miR-320d reduced the expression of GP1BA, HDAC10, FGG, PADI4, MPO, and NE. Mechanistically, miR-320d suppressed NF-κB signaling, as shown by decreased phosphorylated NF-κB (p-NF-κB) and total NF-κB levels, and reduced IL-8 secretion in NPC cells. Conclusion: miR-320d may suppress NPC progression, at least in part, by attenuating NF-κB/IL-8-associated NET formation. These findings suggest that the miR-320d/NF-κB/IL-8/NET regulatory axis may participate in NPC progression and may warrant further translational investigation.

To investigate the effects of Biyan Jiedu Capsules on the proliferation and apoptosis of nasopharyngeal carcinoma cells and their molecular mechanism, nasopharyngeal carcinoma cells CNE1 and CNE2 were used. They were divided into control group(30% blank serum medium), low-(10% drug-containing serum + 20% blank serum medium), medium-(20% drug-containing serum + 10% blank serum medium), and high-(30% drug-containing serum medium) concentration group of Biyan Jiedu Capsules according to in vitro experiment. After 24 h of intervention, the effects of Biyan Jiedu Capsules on the proliferation of CNE1 and CNE2 were detected by CCK-8 assay, clonal formation experiment, and EdU staining. The effect of Biyan Jiedu Capsules on apoptosis of CNE1 and CNE2 was detected by flow cytometry. Western blot was used to detect the effect of Biyan Jiedu Capsules on the expression of X-linked apoptosis inhibitor protein(XIAP), survivin, proliferating cell nuclear antigen(PCNA), and PI3K/Akt pathway-related proteins in CNE1 and CNE2. The results showed that compared with the control group, the survival rate of CNE1 and CNE2 in the medium and high concentration groups of Biyan Jiedu Capsules could be decreased in a concentration-dependent way(P<0.05, P<0.01). At the same time, EdU staining and clonal formation experiments showed that the proliferation of CNE1 and CNE2 was significantly inhibited in the medium and high concentration groups of Biyan Jiedu Capsules(P<0.05, P<0.01). Flow cytometry showed that the apoptosis rate of CNE1 and CNE2 was significantly increased in all concentration groups of Biyan Jiedu Capsules(P<0.01), and the apoptosis rate was concentration-dependent. Western blot showed that the expressions of XIAP, survivin, PCNA, p-PI3K, and p-Akt in all concentration groups of Biyan Jiedu Capsules were significantly down-regulated(P<0.05, P<0.01). In conclusion, Biyan Jiedu Capsules can inhibit the proliferation and induce apoptosis of nasopharyngeal carcinoma cells possibly by down-regulating the PI3K/Akt signaling pathway.

Nasopharyngeal carcinoma is a type of malignant tumour occurring in the nasopharyngeal mucosal epithelium. This carcinoma often has no obvious symptoms in the early stages and is frequently diagnosed at mid-to-advanced stages. Interleukin-6 (IL-6) is a multifunctional cytokine that can participate in the regulation of the immune system, haematopoiesis, induction of acute phase protein secretion, and cell proliferation and differentiation of. IL-6 is a core molecule in tumour inflammation and carcinoma metastasis that promotes various tumours. This article discusses the promoting effects of IL-6 in the occurrence and development of nasopharyngeal carcinoma from the perspectives of release of pro-inflammatory factors, regulation of the tumour microenvironment, enhanced migration and invasion abilities of tumour cells and distant metastasis, and improved tumour immune evasion functions. In addition, important implications of IL-6 for the diagnosis, treatment, and prognosis of nasopharyngeal carcinoma are discussed.

AIM:This retrospective study was aimed to evaluate the diagnostic value of a combination of carbohydrate antigen 19-9 (CA19-9), carcinoembryonic antigen (CEA) and protein induced by vitamin K absence or antagonist-Ⅱ (PIVKA-II) in pancreatic cancer. METHODS:Clinical data were collected from 111 pancreatic cancer patients and 158 patients with benign pancreatic diseases (BPD). Serum CA19-9, CEA and PIVKA-II were subjected to receiver operating characteristic curve (ROC) analysis alone and in combination for the diagnosis of pancreatic cancer. RESULTS:Serum CA19-9, CEA, and PIVKA-II were higher in pancreatic cancer patients than in BPD patients (P < 0.001). ROC analysis indicated that the cutoff values were 99.390 for CA19-9, 3.065 for CEA, and 42.965 for PIVKA-II, at which the positive rate in pancreatic cancer was 78.38 % for CA19-9, 43.24 % for CEA and 48.65 % for PIVKA-Ⅱ. When serum CA19-9, CEA, and PIVKA-II were used alone, the areas under the curves (AUC), sensitivity and specificity were 0.821, 68.47 % and 89.24 % for CA19-9, 0.763, 61.26 % and 85.44 % for CEA, and 0.681, 45.95 % and 87.34 % for PIVKA-II. When serum CA19-9, CEA, and PIVKA-II were used in combination, the positivity rate was 94.59 % in pancreatic cancer with AUC of 0.903, sensitivity of 81.10 % and specificity of 88.00 %. CONCLUSION:PIVKA-II is a potential serum marker of pancreatic cancer and the combination of CA19-9, CEA, and PIVKA-II is a novel panel of serum markers with promising diagnostic value for pancreatic cancer.

Dysregulated RNA processing is crucial in nasopharyngeal carcinoma (NPC) progression. Our research aimed to evaluate the prognostic values of RNA-processing genes (RPGs) in NPC through bioinformatic analysis of the GSE12452 and GSE102349 datasets, identifying differentially expressed RNA-processing genes (DE-RPGs). A prognostic model was developed using univariate and multivariate Cox analysis, with effectiveness assessed by ROC analysis. The correlation between risk scores, immune characteristics, and chemotherapy sensitivity was also analyzed. Model gene expression was validated by RT-qPCR, Western Blot, and immunohistochemistry, alongside functional assays. Bioinformatics indicated that RNA binding motif protein 20 (RBM20) and LSM5 are prognostic RPGs, with the ROC curve confirming their predictive ability for survival. Significant differences in drug sensitivity were noted between high- and low-risk groups. Experimental validation showed LSM5 is overexpressed in NPC tissues, correlating with poorer prognosis, and its down-regulation inhibits cell proliferation and migration. Thus, LSM5 is identified as a new adverse biomarker in NPC, with implications for targeted therapy and prognosis improvement.

Excessive cellular proliferation and metabolic reprogramming are important characteristics of cancer cells.Cancer cells promote excessive proliferation and growth by altering coordinated metabolic pathways.In terms of glucose metabolism,most cancer cells exhibit increased glucose uptake and lactate production even under aerobic conditions,known as the Warburg effect.Increased glucose uptake not only provides energy but also supplies essential carbon sources for the biosynthesis of nucleotides,lipids,and proteins.During this process,decreased pyruvate dehydrogenase activity leads to disruption of the tricarboxylic acid cycle(TCA),thereby increasing tumor cell dependence on other nutrients.In addition to glucose,glutamine(Gln)is also a key metabolic substrate required for cancer cell growth and proliferation.It provides both carbon and nitrogen sources to support the synthesis of ribose,non-essential amino acids,citrate,and glycerol,and compensates for the reduced oxidative phosphorylation caused by the Warburg effect.In human plasma,Gln is one of the most abundant amino acids.Normal cells synthesize Gln through glutaminase(GLS),but the Gln synthesized by tumor cells is insufficient to meet the demands of rapid proliferation,resulting in"Gln dependence".Most cancers,including osteosarcoma,show significantly increased demand for Gln.Metabolic reprogramming enables tumor cells to gain survival advantages in maintaining redox homeostasis and biosynthesis while forming unique metabolic phenotypes.Focusing on key enzymes and transporters involved in Gln metabolism in osteosarcoma and identifying potential targets may provide new ideas and directions for drug development.

This review explores the dual role of miR-195 in cancer, acting as both a tumor suppressor and, in specific contexts, a tumor promoter. It highlights its molecular mechanisms, focusing on key signaling pathways such as Wnt-1/β-catenin, VEGF/VEGFR, and PI3K/AKT/mTOR, as well as its involvement in competitive gene regulation. The clinical potential of miR-195 in cancer screening, diagnosis, prognosis, and therapy is examined, particularly its ability to enhance therapeutic efficacy and reduce recurrence risk when combined with chemotherapy or immunotherapy. Despite these promising aspects, challenges such as precise regulation, efficient delivery systems, and clinical translation remain. Future research should prioritize advancing miR-195’s integration into personalized medicine, immunotherapy, and novel delivery technologies, aiming to establish it as a reliable biomarker and therapeutic target for improved cancer care.

Early diagnosis is vitally important for effective treatment of nasopharyngeal carcinoma (NPC). Nevertheless, the exact pathogenic mechanisms of NPC remain unclear, and early diagnosis of NPC is still limited. Herein, we showed that a specific tsRNA for NPC, 5'tiRNA-32-ValAAC-2, is a novel pathogenic factor and has potential diagnostic value for NPC screening. In this study, small RNA microarray profiling and array hybridization were used to detect expression spectrums of tsRNAs in the sera of newly diagnosed NPC patients. The upregulated tsRNAs were validated using RT-qPCR, and their clinical significance in NPC diagnosis was analyzed. Furthermore, the most highly expressed tsRNA, was further investigated. 5'tiRNA-32-ValAAC-2 could serve as a potential diagnostic biomarker for NPC. Subsequently, the effect of 5'tiRNA-32-ValAAC-2 on the growth and invasion of NPC cells was investigated. The results indicated that overexpression of 5'tiRNA-32-ValAAC-2 promoted NPC cells proliferation, migration, and invasion. In contrast, the inhibition of 5'tiRNA-32-ValAAC-2 suppressed NPC cells proliferation, migration and invasion. TargetScan and miRanda analyses revealed that UGT2B7, SYNPO2, ZNF44, PDHB, and UFM1 might serve as downstream target-genes of 5'tiRNA-32-ValAAC-2. In conclusion, 5'tiRNA-32-ValAAC-2 could potentially be a novel pathogenic factor for NPC, and it functions as a diagnostic biomarker in the primary diagnosis of NPC.

Nasopharyngeal carcinoma (NPC) is a malignant neoplasm that is highly prevalent in East Asia and presents significant therapeutic challenges due to limited treatment options and severe adverse effects. Ursolic acid (UA) is a pentacyclic triterpenoid with anticancer activity in various tumors; however, its mechanism of action in NPC remains unclear. This study integrated network pharmacology with experimental validation to elucidate the molecular mechanism underlying the effect of UA against NPC. Screening of a network pharmacology database identified 39 targets common to UA and NPC, among which P53, STAT3, Bcl-2, IL1B, and CASP3 showed high node degrees in the protein–protein interaction network. Gene Ontology analysis revealed that these targets were primarily enriched in stress response and apoptosis regulation, whereas Kyoto Encyclopedia of Genes and Genomes analysis indicated significant enrichment in the P53 signaling and apoptosis pathways. UA dose-dependently inhibited the proliferation of the NPC cell lines S18 and S26 (p < 0.01), and induced apoptosis, as demonstrated by Annexin V-FITC/PI double fluorescence staining and confirmed by Hoechst 33,342 staining showing nuclear condensation. UA also caused mitochondrial membrane depolarization, as indicated by JC-1 staining. Western blot analysis showed significant upregulation of P53 and the pro-apoptotic protein BAX (p < 0.01), and downregulation of the anti-apoptotic protein Bcl-2 (p < 0.01) following UA treatment. This study is the first to show that UA induces apoptosis in NPC cells by activating the P53 signaling pathway using network pharmacology and experimental validation.

RNA methylation modifications are widespread in eukaryotes and prokaryotes, with N6-methyladenosine (m6A) methylation being the most prevalent internal modification in eukaryotic mRNA and having become a prominent focus of tumor research in recent years. Up to now, substantial evidence has suggested that the dysregulated RNA demethylase ALKBH5 can interact with m6A reader proteins to modulate a wide range of mRNA biological progress, including mRNA shearing, export, metabolism, and stability, ultimately influencing tumorigenesis and development. To deeply understand the regulatory roles of ALKBH5 and reader proteins in tumor progression, this review aims to summarize the structures of ALKBH5 and reader proteins, as well as their cooperative regulatory mechanisms that affect the occurrence and development of tumors originating from different systems. Furthermore, the potential applications of targeting ALKBH5 and reader proteins in antitumor drug development are summarized, hoping to provide a strong basis for advancing antineoplastic research in the future.

This study aimed to investigate the effect and potential mechanism of evodiamine (EVO) on proliferation and apoptosis of nasopharyngeal carcinoma (NPC) cells. EVO inhibited proliferation, blocked cell cycle progression, and induced apoptosis of NPC cells. There are 27 known anti-NPC targets of EVO, of which eight are core targets, namely SRC, ERBB2, STAT3, MAPK8, NOS3, CXCL8, APP, and HDAC1. Molecular docking analysis showed that the binding of EVO with its key targets (SRC, ERBB2) was good. EVO also reduced the expression of SRC and ERBB2, the key proteins p-MEK and p-ERK1/2 of the MAPK/ERK signaling pathway, and the downstream proteins PCNA and XIAP. EVO inhibited the growth of NPC xenografts in nude mice and reduced the expression levels of SRC, ERBB2, ERK1/2, p-ERK1/2, PCNA and XIAP in NPC tissue. When the MAPK/ERK signaling pathway was activated by epidermal growth factor (EGF), the expression levels of PCNA and XIAP increased, the cell proliferation index increased, and the apoptosis rate decreased in the EGF + EVO treatment group compared to treatment with EVO alone. These changes indicated that the inhibitory effect of EVO on proliferation and apoptosis of NPC cells was related to the down-regulation of SRC and ERBB2 expression, and further inhibition of the MAPK/ERK signaling pathway.

ObjectiveThis study aims to assess the current research status, focus areas, and developmental trends in nasopharyngeal carcinoma (NPC) through a bibliometric analysis. MethodsArticles focusing on NPC published from 2000 to 2023 were retrieved from the Web of Science database. VOSviewer and CiteSpace were used for bibliometric and visual analysis. ResultsA total of 14516 related publications were retrieved. There has been a steady increase in the number of NPC-related publications from 2000 to 2023. China was the dominant country in this field with 8948 papers (61.64%), followed by the USA (2234, 15.39%). Sun Yat-sen University was the most influential institution, while Ma J was the most prolific author. Furthermore, Head And Neck-journal For The Sciences And Specialties Of The Head And Neck was the most prolific journal. International Journal of Radiation Oncology Biology Physics had the highest total citation counts. "Introduction chemotherapy", "Concurrent chemotherapy", "Epithelial-mesenchymal transition", "Cancer stem cells", "MicroRNAs", "LncRNA", "Exosomes", and "Biomarker" were the most common keywords. The reference "Chen YP, 2019, Lancet" had the highest citations and strong outbreak value. ConclusionThe past two decades have witnessed a significant increase in research on NPC. The optimization of treatment mode is the most widely studied aspect at present. The mechanism of occurrence and development and the most favorable diagnostic and therapeutic targets are the research hotspots in the future.

鼻咽癌是一种起源于鼻咽黏膜的上皮性癌,在我国主要高发于南方地区.miRNA是一类非编码的小RNA分子,在组织、血清、血浆和其他体液中稳定性表达,通过与互补的靶mRNA结合,导致mRNA翻译抑制或mRNA降解,在细胞增殖、分化过程中发挥核心作用,并在恶性肿瘤的发生、发展中发挥着促癌或抑癌作用.miRNA异常表达可通过改变癌基因和抑癌基因的表达来参与鼻咽癌的发生、转移和耐药性,在鼻咽癌的诊断和治疗中具有重要作用.研究异常表达的miRNA及其作用机制,进一步阐明鼻咽癌的发病机制,可为鼻咽癌的诊断和治疗提供新的研究方向.本文对近年来miRNA在鼻咽癌的发生、发展、诊断、治疗和预后评估中的作用进行综述,以期为miRNA调控鼻咽癌的基础研究及其转化应用提供科学依据和新思路.

目的 探究在中医耳鼻咽喉科学课程教学中挖掘和融入思政元素的教学途径.方法 结合中医耳鼻咽喉科学课程的教学现状和特点探索、挖掘其中存在的思政元素,并设计多元化的教学途径将思政元素融入到中医耳鼻喉科学课程中去,从整体上提高中医耳鼻咽喉科的教学质量、改善和培养医学生的思政素养、人文素质、综合技能.结果 在中医耳鼻咽喉科教学过程中通过多种途径融入思政元素,可以更好地达到培养医学生科学价值观、政治素养及综合素质的教学目的,帮助中医耳鼻咽喉科教学工作者积累更多的教学经验.结论 在中医耳鼻咽喉科学课程教学中通过挖掘其中