Two-Sex Life Table Analysis for Optimizing Beauveria bassiana Application against Spodoptera exigua (Hübner) (Lepidoptera: Noctuidae).

Spodoptera exigua (Hübner) (Lepidoptera: Noctuidae) is a highly dispersive, polyphagous insect pest that severely defoliates crops. Excessive reliance on synthetic insecticides leads to ecological pollution and resistance development, urging scientists to probe eco-friendly biopesticides. Here, we explore the virulence of an entomopathogenic fungus, Beauveria bassiana, against S. exigua, resulting in 88% larval mortality. Using an age-stage, two-sex life table, we evaluated the lethal and sublethal effects of B. bassiana on the demographic parameters of S. exigua, including survival, development, and reproduction. Sublethal (LC20) and lethal concentrations (LC50) of B. bassiana impacted the parental generation (F0), with these effects further influencing the demographic parameters of the first filial generation (F1). The infected F1 offsprings showed a reduced intrinsic rate of increase (r), mean generation time (T), and net reproduction rate (R0). Larval developmental duration varied significantly between the control (10.98 d) and treated groups (LC20: 10.42; LC50: 9.37 d). Adults in the treated groups had significantly reduced lifespans (M: 8.22; F: 7.32 d) than the control (M: 10.00; F: 8.22 d). Reduced fecundity was observed in the B. bassiana-infected groups (LC20: 313.45; LC50: 223.92 eggs/female) compared to the control (359.55 eggs/female). A biochemical assay revealed elevated levels of detoxification enzymes (esterases, glutathione S-transferases, and acetylcholinesterase) in the F0 generation after B. bassiana infection. However, the enzymatic activity remained non-significant in the F1 generation likely due to the lack of direct fungal exposure. Our findings highlight the enduring effects of B. bassiana on the biological parameters and population dynamics of S. exigua, stressing its use in eco-friendly management programs.

ARHGAP10, Transcriptionally Regulated by Sodium Butyrate, Promotes Ferroptosis of Ovarian Cancer Cells.

BACKGROUND: Ovarian cancer is a highly lethal gynecologic malignancy. ARHGAP10, a member of Rho GTPase-activating proteins, is a potential tumor suppressor in ovarian cancer. However, its role and the involved mechanism need further examination. Here, we investigated whether ARHGAP10 is also associated with ferroptosis. METHODS: Lentivirus infection was used for gene overexpression or silencing. Real-time polymerase chain reaction (RT-PCR) and Western blot were used to assess mRNA and protein levels, respectively. Cell viability was assessed by Cell Counting Kit-8 (CCK-8) assay. Lipid reactive oxygen species level was measured by flow cytometry. A tumorigenicity assay was performed to evaluate tumor growth in vivo, and sections of mouse tumor tissues were examined by immunofluorescence microscopy. Chromatin Immunoprecipitation (ChIP) assay was used to assess the binding of H3K9ac to the promoter region of ARHGAP10. RESULTS: ARHGAP10 overexpression promoted ferroptosis in ovarian cancer cells, resulting in decreased cell viability, and increased lipid reactive oxygen species (ROS) level. Further, it decreased and increased GPX4 and PTGS2 expression, respectively, and also induced suppression of tumor growth in mice. Fer-1, a potent inhibitor of ferroptosis, suppressed the above effects of ARHGAP10. Contrarily, ARHGAP10 silencing alleviated ferroptosis in ovarian cancer cells, which was reversed by RSL3, a ferroptosis-inducing agent. Lastly, sodium butyrate (SB) was found to transcriptionally regulate ARHGAP10, thereby also contributing to the ferroptosis of ovarian cancer cells. CONCLUSIONS: Our results suggest that SB/ARHGAP10/GPX4 is a new signaling axis involved in inducing ferroptosis in ovarian cancer cells and suppressing tumor growth, which has potential clinical significance.

Levomilnacipran Improves Lipopolysaccharide-Induced Dysregulation of Synaptic Plasticity and Depression-Like Behaviors via Activating BDNF/TrkB Mediated PI3K/Akt/mTOR Signaling Pathway.

Depression is a common psychological disease with high morbidity and mortality. Recently, the involvement of synaptic plasticity in the pathogenesis of depression has shed light on the direction of developing novel antidepressants. Levomilnacipran is a newly approved medication for the treatment of adult major depressive disorder. However, the detailed mechanisms underlying its antidepressant-like effects have yet to be illuminated. In this study, we aimed to investigate the role of levomilnacipran in regulating synaptic plasticity and explore the possible molecular mechanisms of its antidepressant effects using a rat model of depression induced by lipopolysaccharide (LPS). The results demonstrated that levomilnacipran (30 mg/kg, i.p.) significantly ameliorated depression-like behaviors in rats, alleviated the dysregulation of synaptic plasticity, and suppressed neuroinflammation within hippocampus induced by LPS-treatment. Levomilnacipran increased the expression of postsynaptic dense 95 (PSD-95) and synaptophysin (Syn) and reversed the imbalance between pro- and anti-inflammatory cytokines within hippocampus of depressed rats. Additionally, levomilnacipran elevated expression level of brain-derived neurotrophic factor (BDNF), accompanied by increased tyrosine kinase B (TrkB), phosphorylated phosphatidylinositol 3-kinase (PI3K), phosphorylated protein kinase B (p-Akt), and phosphorylated mammalian target of rapamycin (p-mTOR). Taken together, these results suggest that levomilnacipran may exert antidepressant effects via upregulating BDNF/TrkB mediated PI3K/Akt/mTOR signaling pathway to improve synaptic plasticity. These findings reveal potential mechanisms for the antidepressant effects of levomilnacipran and offer new insights into the treatments for depression.

Levomilnacipran ameliorates lipopolysaccharide-induced depression-like behaviors and suppressed the TLR4/Ras signaling pathway.

Levomilnacipran, a serotonin and norepinephrine reuptake inhibitor, has been reported to have anti-depressive effects. However, the detailed mechanisms underlying these effects are still unclear. This study aimed to investigate the antidepressant mechanisms of levomilnacipran to discover new perspectives on the treatment of depression in male rats. Intraperitoneal injection of lipopolysaccharide (LPS) was used to induce depressive behaviors in rats. Activation of microglia and apoptosis of neurons verified by immunofluorescence. Inflammatory related proteins and neurotrophic related proteins were verified by immunoblotting. The mRNA expression of apoptosis markers was verified by real-time quantitative PCR. Finally, electron microscopy analysis was used to observe the ultrastructural pathology of neuron. Here, we found that the anti-depression and anti-anxiety effects of levomilnacipran in the LPS-induced rat model of depression was resulted from the suppression of neuroinflammation and neuronal apoptosis within prefrontal cortex of rats. Furthermore, we found that levomilnacipran could decrease the number of microglia and suppress its activation in prefrontal cortex of rats. This effect may be mediated by suppressing the TLR4/NF-κB and Ras/p38 signaling pathways. In addition, levomilnacipran plays a neuroprotective role by increasing the expression of neurotrophic factors. Taken together, these results suggest that levomilnacipran exerts antidepressant effects by attenuating neuroinflammation to inhibit the damage in central nervous system and plays a neuroprotective role to improve depressive behaviors. These findings suggest that suppression of neuroinflammation in prefrontal cortex could ameliorate depressive behavioral disorder of rats induced by LPS, which provided a new perspective for the treatment of depression.

The relationship between autophagy and PD-L1 and their role in antitumor therapy.

Immune checkpoint blockade therapy is an important advance in cancer treatment, and the representative drugs (PD-1/PD-L1 antibodies) have greatly improved clinical outcomes in various human cancers. However, since many patients still experience primary resistance, they do not respond to anti-PD1/PD-L1 therapy, and some responders also develop acquired resistance after an initial response. Therefore, combined therapy with anti-PD-1/PD-L1 immunotherapy may result in better efficacy than monotherapy. In tumorigenesis and tumor development processes, the mutual regulation of autophagy and tumor immune escape is an intrinsic factor of malignant tumor progression. Understanding the correlation between the tumor autophagy pathway and tumor immune escape may help identify new clinical cancer treatment strategies. Since both autophagy and immune escape of tumor cells occur in a relatively complex microenvironmental network, autophagy affects the immune-mediated killing of tumor cells and immune escape. Therefore, comprehensive treatment targeting autophagy and immune escape to achieve "immune normalization" may be an important direction for future research and development. The PD-1/PD-L1 pathway is essential in tumor immunotherapy. High expression of PD-L1 in different tumors is closely related to poor survival rates, prognoses, and treatment effects. Therefore, exploring the mechanism of PD-L1 expression is crucial to improve the efficacy of tumor immunotherapy. Here, we summarize the mechanism and mutual relationship between autophagy and PD-L1 in antitumor therapy, which may help enhance current antitumor immunotherapy approaches.

Improving the Neural Segmentation of Blurry Serial SEM Images by Blind Deblurring.

Serial scanning electron microscopy (sSEM) has recently been developed to reconstruct complex largescale neural connectomes, through learning-based instance segmentation. However, blurry images are inevitable amid prolonged automated data acquisition due to imprecision in autofocusing and autostigmation, which impose a great challenge to accurate segmentation of the massive sSEM image data. Recently, learning-based methods, such as adversarial learning and supervised learning, have been proven to be effective for blind EM image deblurring. However, in practice, these methods suffer from the limited training dataset and the underrepresentation of high-resolution decoded features. Here, we propose a semisupervised learning guided progressive decoding network (SGPN) to exploit unlabeled blurry images for training and progressively enrich high-resolution feature representation. The proposed method outperforms the latest deblurring models on real SEM images with much less ground truth input. The improvement of the PSNR and SSIM is 1.04 dB and 0.086, respectively. We then trained segmentation models with deblurred datasets and demonstrated significant improvement in segmentation accuracy. The A-rand (Bogovic et al. 2013) decreased by 0.119 and 0.026, respectively, for 2D and 3D segmentation.

Hypoxic glioma-derived extracellular vesicles harboring MicroRNA-10b-5p enhance M2 polarization of macrophages to promote the development of glioma.

INTRODUCTION: The delivery of biomolecules by tumor cell-secreted extracellular vesicles (EVs) is linked to the development of glioma. Here, the present study was implemented to explore the functional significance of hypoxic glioma cell-derived EVs carrying microRNA-10b-5 (miR-10b-5p) on glioma with the involvement of polarization of M2 macrophages. METHODS: EVs were isolated from hypoxia-stimulated glioma cells, and their role in polarization of M2 macrophages was studied by co-culturing with macrophages. miR-10b-5p expression in glioma tissues, glioma-derived EVs, and macrophages co-cultured with EVs was characterized. Interaction among miR-10b-5p, NEDD4L, and PIK3CA was analyzed. The macrophages or glioma cells were transfected with overexpressing plasmid or shRNA to study the effects of miR-10b-5p/NEDD4L/PIK3CA on M2 macrophage polarization, and glioma cell proliferation, migration, and invasion in vitro and in vivo. RESULTS: Promotive role of hypoxia-stimulated glioma-derived EVs in macrophage M2 polarization was confirmed. Elevation of miR-10b-5p occurred in glioma tissues, glioma-derived EVs and macrophages co-cultured with EVs, and stimulated M2 polarization of macrophages. NEDD4L was a target gene of miR-10b-5p. Overexpression of NEDD4L could inhibit PI3K/AKT pathway through increase in ubiquitination and degradation of PIK3CA. Hypoxic glioma-derived EVs harboring upregulated miR-10b-5p triggered an M2 phenotype in macrophages as well as enhanced aggressive tumor biology of glioma cells via inhibition of PIK3CA/PI3K/AKT pathway by targeting NEDD4L. CONCLUSIONS: In summary, miR-10b-5p delivered by hypoxic glioma-derived EVs accelerated macrophages M2 polarization to promote the progression of glioma via NEDD4L/PIK3CA/PI3K/AKT axis.

Respiratory Prediction Based on Multi-Scale Temporal Convolutional Network for Tracking Thoracic Tumor Movement.

Radiotherapy is one of the important treatments for malignant tumors. The precision of radiotherapy is affected by the respiratory motion of human body, so real-time motion tracking for thoracoabdominal tumors is of great significance to improve the efficacy of radiotherapy. This paper aims to establish a highly precise and efficient prediction model, thus proposing to apply a depth prediction model composed of multi-scale enhanced convolution neural network and temporal convolutional network based on empirical mode decomposition (EMD) in respiratory prediction with different delay times. First, to enhance the precision, the unstable original sequence is decomposed into several intrinsic mode functions (IMFs) by EMD, and then, a depth prediction model of parallel enhanced convolution structure and temporal convolutional network with the characteristics specific to IMFs is built, and finally training on the respiratory motion dataset of 103 patients with malignant tumors is conducted. The prediction precision and time efficiency of the model are compared at different levels with those of the other three depth prediction models so as to evaluate the performance of the model. The result shows that the respiratory motion prediction model determined in this paper has superior prediction performance under different lengths of input data and delay time, and, furthermore, the network update time is shortened by about 60%. The method proposed in this paper will greatly improve the precision of radiotherapy and shorten the radiotherapy time, which is of great application value.

Agomelatine rescues lipopolysaccharide-induced neural injury and depression-like behaviors via suppression of the Gαi-2-PKA-ASK1 signaling pathway.

BACKGROUND: Agomelatine has been shown to be effective in the treatment of depression, but the molecular mechanisms underlying its antidepressant effects have yet to be elucidated. Identification of these molecular mechanisms would not only offer new insights into the basis for depression but also provide the foundation for the development of novel treatments for this disorder. METHODS: Intraperitoneal injection of LPS was used to induce depression-like behaviors in rats. The interactions of the 5-HT2C reporter and Gαi-2 were verified by immunoprecipitation or immunofluorescence assay. Inflammatory related proteins, autophagy related proteins and apoptosis markers were verified by immunoblotting or immunofluorescence assay. Finally, electron microscopy analysis was used to observe the synapse and ultrastructural pathology. RESULTS: Here, we found that the capacity for agomelatine to ameliorate depression and anxiety in a lipopolysaccharide (LPS)-induced rat model of depression was associated with an alleviation of neuroinflammation, abnormal autophagy and neuronal apoptosis as well as the promotion of neurogenesis in the hippocampal dentate gyrus (DG) region of these rats. We also found that the 5-HT2C receptor is coupled with G alphai (2) (Gαi-2) protein within hippocampal neurons and, agomelatine, acting as a 5-HT2C receptor antagonist, can up-regulate activity of the Gαi-2-cAMP-PKA pathway. Such events then suppress activation of the apoptosis signal-regulating kinase 1 (ASK1) pathway, a member of the mitogen-activated protein kinase (MAPK) family involved in pathological processes of many diseases. CONCLUSION: Taken together, these results suggest that agomelatine plays a neuroprotective role in regulating neuroinflammation, autophagy disorder and apoptosis in this LPS-induced rat model of depression, effects which are associated with the display of antidepressant behaviors. These findings provide evidence for some of the potential mechanisms for the antidepressant effects of agomelatine.

Inhibition of NF-κB activation by BAY 11-7821 suppresses the proliferation and inflammation of glioma cells through inducing autophagy.

Background: Gliomas have been known as the most common intracranial malignant tumor, and this kind of tumors cause huge amounts of mortality. The NF-κB inhibitor BAY 11-7821 has been reported as a novel approach in the immunotherapy of lung diseases. However, the functional role of BAY 11-7821 and its association with autophagy in glioma cells have not yet been reported. Methods: In this study, 2 glioma cell lines (U87 and U251) were treated with different doses of BAY 11-7821, or combined with authphagy inhibitor, 3-MA. Afterwards, Transwell assay, CCK-8 assay, EdU staining, Western blot and immunofluorescence assay was used to detected the cell migration, invasion, vability, autophagy in U87 and U251. Results: Our data showed that BAY 11-7821 significantly suppressed the viability, proliferation, migration, and invasion of glioma cells in a dose-dependent manner. At the molecular level, BAY 11-7821 downregulated the protein levels of p-IκBα, p-p65, NLRP3, and p62, and upregulated the protein levels of caspase 3 and Bax, as well as decreased the levels of IL-1ß and IL-18. Results showed BAY 11-7821 enhanced autophagy. While, Pre-treatment with 3-MA, an autophagy inhibitor, obviously reversed the effects of BAY 11-7821 on malignant biological behaviors of glioma cell, inflammation status, and autophagy. Conclusions: In this study, we found that BAY 11-7821 has an effective inhibitive function on malignant biological behaviors by mediating autophagy. Our findings contribute to a better understanding of BAY 11-7821 as a potential anticancer drug in glioma via activating autophagy.

An Overview of EEG-based Machine Learning Methods in Seizure Prediction and Opportunities for Neurologists in this Field.

The unpredictability of epileptic seizures is one of the most problematic aspects of the field of epilepsy. Methods or devices capable of detecting seizures minutes before they occur may help prevent injury or even death and significantly improve the quality of life. Machine learning (ML) is an emerging technology that can markedly enhance algorithm performance by interpreting data. ML has gained increasing attention from medical researchers in recent years. Its epilepsy applications range from the localization of the epileptic region, predicting the medical or surgical outcome of epilepsy, and automated electroencephalography (EEG) analysis to seizure prediction. While ML has good prospects with regard to detecting epileptic seizures via EEG signals, many clinicians are still unfamiliar with this field. This work briefly summarizes the history and recent significant progress made in this field and clarifies the essential components of the automatic seizure detection system using ML methodologies for clinicians. This review also proposes how neurologists can actively contribute to ensure improvements in seizure prediction using EEG-based ML.

The Value of Vaginal Microbiome in Patients with Endometrial Hyperplasia.

Objective: To investigate the profiles of the vaginal microbiome in patients with endometrial hyperplasia and to explore the potential value of vaginal microbiome in the diagnosis of endometrial hyperplasia. Materials/Methods. 26 patients suffering from abnormal uterine bleeding (AUB) with thickened endometrium revealed by transvaginal ultrasonography were enrolled. Based on pathology, 12 patients with endometrial hyperplasia were classified as the Veh group and 14 patients with proliferative endometrium were classified as the Vne group. The vaginal samples were collected for the presence of microbial DNA by high-throughput next-generation sequencing of the 16S rRNA gene. The α-diversity and ß-diversity of vaginal microbiome were analyzed and compared between bacterial populations. The ROC curve was made to evaluate the feasibility of flora as a biomarker. Results: The diversity of vaginal microbiome in the Veh group was significantly lower than that in the Vne group (P < 0.05). Lactobacillus was the most represented genus in the Veh group. The study's t-test between the two groups showed that Lactobacillus has the only significant difference in the abundance of the first 15 genera (P < 0.01). ROC analysis of the abundance of Lactobacillus showed that the area of AUC was 0.83, the sensitivity was 93.00%, and the specificity was 75.00%. Conclusion: The study offers insight into the nature of the vaginal microbiome and suggests that surveying the vaginal microbiota might be useful for detection of endometrial hyperplasia.

EZH2-Inhibited MicroRNA-454-3p Promotes M2 Macrophage Polarization in Glioma.

Glioma is a primary intracranial tumor with high incidence and mortality. The oncogenic role of EZH2 has been reported in glioma. EZH2 inhibited microRNA-454-3p (miR-454-3p) by binding to its promoter in chondrosarcoma cells. Therefore, our study aimed to identify whether EZH2 regulated M2 macrophage polarization in glioma via miR-454-3p. Clinical samples of different grades of glioma and glioma cells were collected and immunohistochemistry and RT-qPCR demonstrated that EZH2 was highly expressed in glioma tissues. Expression of EZH2 was positively correlated with the degree of M2 macrophage polarization in glioma tissues. EZH2 was silenced by lentivirus in glioma cells, which were subsequently co-cultured with macrophages to evaluate its effect on macrophage polarization. miR-454-3p, a down-regulated miR in glioma, was found to be increased after silencing of EZH2. Furthermore, MethPrimer analysis showed that EZH2 silencing inhibited the DNA methylation level of miR-454-3p. Additionally, MS-PCR, dual-luciferase reporter, RIP and RNA pull down assays revealed that miR-454-3p promoted PTEN expression by inhibiting m6A modification through binding to the enzyme YTHDF2. Either inhibition of miR-454-3p or PTEN resulted in promotion of M2 macrophage polarization. Collectively, histone methyltransferase EZH2 inhibited miR-454-3p through methylation modification and promoted m6A modification of PTEN to induce glioma M2 macrophage polarization.

Risk factor analysis of bronchospasm after tracheobronchial foreign body removal: Cases report and literature review (STROBE).

ABSTRACT: This retrospective study aimed to investigate bronchospasm after tracheobronchial foreign body removal. Bronchoscopy is the main clinical treatment for removing airway foreign bodies, but postoperative airway spasm is very common. In our study, we perform a risk factor analysis of bronchospasm after tracheobronchial foreign body removal. The sample was composed of 261 children with airway foreign bodies who had undergone clinical bronchoscopy for foreign body removal under general anesthesia were enrolled from the department of otolaryngology, the First Hospital of Jilin University from 2014 to 2019, of which 78 in the left bronchus, 107 in the right bronchus, 51 in the main bronchus, and 25 in the subglottis. All patients were confirmed by radiographic examination or pulmonary auscultation. All their medical records and clinical data were retrospectively analyzed; single factor and multiple factor analyses of bronchospasm were performed. The logistic regression analysis showed that age, foreign body retention time and operation time were independent risk factors for postoperative airway spasm. A history of pneumonia was not an independent risk factor for postoperative airway spasm. We should pay more attention in the preoperative period according to the specific situation of child; the right means of anesthesia and appropriate hormonal drugs should be chosen to prevent the occurrence of postoperative airway spasm.

Multiple symmetric lipomatosis with secondary laryngeal obstruction: A case report.

INTRODUCTION: Multiple symmetric lipomatosis (MSL) is an uncommon medical condition characterized by symmetric fat accumulation mainly in the neck and other upper body regions. The involvement of the larynx is rare according to the literature, and we present a case of MSL with larynx involvement treated with a surgical approach. PATIENT CONCERNS: A 55-year-old male was admitted to our hospital due to progressively aggravated breathing difficulty, and tracheotomy was performed before transfer. When he tried to block the cannula, the breathing difficulty returned. The patient's neck had been thickening for the past 2 years. DIAGNOSIS: Pathological examination confirmed the diagnosis of MSL. INTERVENTIONS: The patient underwent lumpectomy and neck exploration. OUTCOMES: The lipoma was removed, the patient was free of any dyspnea symptoms and recovered well, and the tracheal cannula was removed at a local hospital. CONCLUSION: MSL can infiltrate the larynx and grow into the preepiglottic space and paraglottic spaces, resulting in breathing difficulties. Lipomas present in the spaces described above must be removed at the same time; otherwise, symptoms of dyspnea cannot be alleviated.

Appearance of cerebellar cyst following microvascular decompression to treat hemifacial spasm: a report of two cases and literature review.

Microvascular decompression (MVD) is an effective and safe approach for treating hemifacial spasm (HFS). Postoperative complications may include facial nerve palsy, hearing loss, intracerebral haematoma, and brainstem infarction. The occurrence of intracranial cyst following MVD is extremely rare, with few cases documented in the literature. Herein, the cases of two patients with HFS who developed ipsilateral cerebellar cyst following MVD are reported. The first patient was a 50-year-old male presenting with a 6-year history of HFS on the right side of his face. MVD was performed, and 12 days postoperatively he developed dizziness and nausea. Magnetic resonance imaging (MRI) showed a cyst in the ipsilateral cerebellum. Antibiotic treatment provided no benefit, and the cyst was drained. The second patient was a 44-year-old female presenting with a 4-year history of HFS on the right side of her face. MVD was performed, and 18 days following surgery, she developed dizziness and nausea. MRI showed an ipsilateral cerebellar cyst. Conservative treatment was applied and the cyst shrunk. At the 2-month follow-up appointment, symptoms were completely resolved in both patients. Cerebellar cyst is a rare complication following MVD. Timely diagnosis and appropriate treatment should be emphasized, and surgical treatment may be unnecessary.

Advances in Understanding CREB Signaling-Mediated Regulation of the Pathogenesis and Progression of Epilepsy.

Recent studies have indicated that the transcription factor cyclic adenosine monophosphate response element binding protein (CREB) is involved in the etiology of epilepsy. With regard to its transcriptional regulation, CREB phosphorylation is critical for the transmission of multiple extracellular signals, which implicates the activation of downstream target genes in the pathogenesis and progression of epilepsy. This review mainly focuses on recent discoveries of associations between the molecular and structural characteristics of CREB as well as the related CREB signaling pathway and epilepsy.

Laryngeal adenoid cystic carcinoma: Three cases reports.

INTRODUCTION: Laryngeal adenoid cystic carcinoma (LACC) is an extremely rare malignant neoplasm. The etiology of LACC remains unknown, and it is characterized by multiple recurrences, slow progression, and late distant metastasis. This study aimed to provide more information regarding the characteristics, diagnosis, and treatment of LACC by analyzing 3 clinical cases and reviewing the literature on this topic. PATIENT CONCERNS: Here, we present all 3 cases of LACC within the period between 2010 and 2019. Dyspnea was the most commonly observed symptom in these patients, followed by hoarseness, pharyngeal paresthesia, and difficulty swallowing. DIAGNOSIS: All patients were pathologically confirmed as LACC. INTERVENTIONS: All the patients underwent a combined therapy of surgical resection plus external irradiation. OUTCOMES: The follow-up time was between 2 and 6 years; no local recurrence occurred in any of the 3 patients. Lung metastasis was found in 1 patient 6 years after surgery. CONCLUSION: LACC is usually a slowly progressing cancer; the main treatment methods are surgery and radiotherapy, and the adequate radiotherapy dose should usually be greater than 60 Gy. The 5-year disease-specific survival rate is high; however, distant metastasis may still occur in patients with LACC even beyond 5 years after treatment. Therefore, patients with LACC require long-term surveillance.