Inhibition of non-small cell lung cancer metastasis by knocking down APE1 through regulating myeloid-derived suppressor cells-induced immune disorders.

BACKGROUND: Non-small cell lung cancer (NSCLC) represents a highly immunogenic malignancy. Immunologic tolerance facilitated by myeloid-derived suppressor cells (MDSCs) is implicated in primary or secondary resistance mechanisms in NSCLC. The potential role of APE1 in regulating NSCLC metastasis by targeting MDSCs remains uncertain. METHODS: This study utilized a plasmid, Plxpsp-mGM-CSF, to induce elevated granulocyte-macrophage colony-stimulating factor (GM-CSF) expression in A549 cells. Tumor transplantation experiments involved A549, A549+GM-CSF, and A549+GM-CSF-siAPE1 cell lines. Evaluation encompassed MDSCs, Treg cells, IgG, CD3, and CD8 levels. RESULTS: Notably, lung cancer tissues and cells displayed markedly reduced APE1 expression. siAPE1 transfection significantly curtailed tumor growth compared to the A549+GM-CSF group. APE1 knockdown orchestrated immune system modulation in lung tumor mice, characterized by diminished MDSCs but augmented Treg cells, IgG, CD3, and CD8. Additionally, APE1 knockdown led to reduced levels of pro-MDSC cytokines (HGF, CCL5, IL-6, CCL12) and a concurrent upregulation of the anti-MDSC cytokine IL-1ra. Furthermore, APE1 knockdown impeded cell viability in both A549 and H1650 cells. CONCLUSIONS: Transplantation of A549-GM-CSF amplified MDSC levels, fostering accelerated tumor growth, while mitigating MDSC levels through APE1 knockdown hindered tumor progression and alleviated inflammatory infiltration in lung cancer tissues. Strategies targeting the APE1/MDSC axis offer a promising approach for lung cancer prevention and treatment, presenting novel insights for NSCLC management.

Intrathecal administration of a novel siRNA modality extends survival and improves motor function in the SOD1G93A ALS mouse model.

Antisense oligonucleotides (ASOs) were the first modality to pioneer targeted gene knockdown in the treatment of amyotrophic lateral sclerosis (ALS) caused by mutant superoxide dismutase 1 (SOD1). RNA interference (RNAi) is another mechanism of gene silencing in which short interfering RNAs (siRNAs) effectively degrade complementary transcripts. However, delivery to extrahepatic tissues like the CNS has been a bottleneck in the clinical development of RNAi. Herein, we identify potent siRNA duplexes for the knockdown of human SOD1 in which medicinal chemistry and conjugation to an accessory oligonucleotide (ACO) enable activity in CNS tissues. Local delivery via intracerebroventricular or intrathecal injection into SOD1G93A mice delayed disease progression and extended animal survival with superior efficacy compared with an ASO resembling tofersen in sequence and chemistry. Treatment also prevented disease-related declines in motor function, including improvements in animal mobility, muscle strength, and coordination. The ACO itself does not target any specific complementary nucleic acid sequence; rather, it imparts benefits conducive to bioavailability and delivery through its chemistry. The complete conjugate (i.e., siRNA-ACO) represents a novel modality for delivery of duplex RNA (e.g., siRNA) to the CNS that is currently being tested in the clinic for treatment of ALS.

Rare Trichilemmal Cyst Localized in the Pulp of the Middle Finger.

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Pathological complete response to neoadjuvant lorlatinib in a patient with unresectable ALK-Positive locally advanced non-small cell lung cancer: A case report.

Anaplastic lymphoma kinase tyrosine kinase inhibitors (ALK-TKIs) have demonstrated substantial effectiveness in individuals with advanced ALK-positive non-small cell lung cancer (NSCLC). However, the controversy over using ALK-TKIs for neoadjuvant therapy in ALK-positive NSCLC has not been fully explored. This case study describes the clinical progression of a patient initially diagnosed with unresectable stage III (cT1bN2M0) lung adenocarcinoma, who was later discovered to harbor an ALK mutation through next-generation sequencing. The patient underwent surgery to achieve a radical resection of the right upper lung lesion after neoadjuvant therapy with lorlatinib and a pathological complete response (pCR) was confirmed by pathological analysis. To our knowledge, it has never been reported that neoadjuvant therapy with lorlatinib resulted in pCR for an ALK-positive patient with stage III NSCLC who was initially unresectable. Therefore, our findings indicate that utilizing ALK-TKIs as neoadjuvant therapy could be considered a viable choice for ALK-positive NSCLC patients.

Correlation Analysis of the TP53 Mutation With Clinical Characteristics in the Prognosis of Non-Small Cell Lung Cancer.

Background: Non-small cell lung cancer (NSCLC) with TP53 mutations has a worse prognosis. It was generally more resistant to chemotherapy and radiation. Our aim was to investigate the correlation between the TP53 co-mutated gene and clinical features, and prognostic value in patients with NSCLC. Methods: Seventy-three patients with a diagnosis of NSCLC at our hospital were recruited. They were divided into the TP53 mutation status (minor) (TP53 MU) and TP53 wild-type (major) (TP53 WT) groups according to their clinical characteristics after their mutation data and clinical information were collected. Serum markers were compared between groups using Mann-Whitney U test. Other clinical factors were compared between groups using χ2 test and Fisher exact test. The log-rank test was used to compare survival curves. Results: Of the 73 patients with NSCLC, 37 (50.68%) were found to carry TP53 mutation. TP53 MU and TP53 WT groups (n = 36) showed a significant difference in the number of smokers, incidence of squamous cell carcinoma, EGFR mutation, and number of advanced patients (P < .05), while gender, age, lymph node metastasis, and KRAS mutation did not differ significantly between the 2 groups. The survival curves in the TP53/KRAS and the TP53/EGFR co-mutation groups suggest that patients with NSCLC may have a shorter progression-free survival (PFS) if they carry one of the 2 types of co-mutation. Conclusions: TP53 gene mutations are more common in patients with NSCLC and squamous cell carcinoma. New predictive markers for NSCLC prognosis may be TP53/KRAS and TP53/EGFR co-mutations.

Thoracoscopic esophagectomy for thoracic esophageal cancer with right aortic arch and Kommerell diverticulum: a case report and literature review.

Background: Esophageal carcinoma accompanied by a right aortic arch (RAA) is very rare. When combined with Kommerell diverticulum (KD), a right aortic arch forms a vascular ring encircling both the esophagus and trachea. Due to abnormal anatomy of the upper mediastinum, it is very difficult to dissociate the esophagus and its surrounding tissues, especially the left recurrent laryngeal nerve. Herein, we report a case of successful thoracoscopic esophagectomy in an esophageal cancer patient concurrent with a RAA and KD. Case presentation: A 62-year-old male patient was diagnosed with esophageal squamous carcinoma in the middle esophagus at clinical stage I (cT1N0M0) according to UICC-TNM classification 8th edition. Further examinations revealed RAA and KD. Based on the three-dimensional CT (3D-CT) reconstruction, a Mckeown esophagectomy via a left thoracoscopic approach in semi-prone position was performed. During the operation, the left recurrent laryngeal nerve was accurately exposed and well protected. Postoperatively, severe complications, including anastomotic leakage and recurrent laryngeal nerve palsy, were not observed. The patient was discharged 12 days after the surgery. Conclusion: Preoperative 3D-CT reconstruction is useful to clarify the vascular malformation in esophageal cancer patients with RAA, and helpful to formulate a reasonable surgical approach.

ACTH-producing small cell neuroendocrine carcinoma from the gallbladder: a case report and literature review.

Ectopic adrenocorticotropic hormone syndrome (EAS) is a condition of hypercortisolism caused by non-pituitary tumors that secrete adrenocorticotropic hormone (ACTH). A rare occurrence of this syndrome is due to an ACTH-producing neuroendocrine tumor that originates from the gallbladder. One patient with severe hypokalemia and alkalosis was admitted to our hospital. Clinical presentations and radiographic findings confirmed the diagnosis of an aggressive ACTH-producing gallbladder malignancy with multiple liver metastases. The diagnosis was verified by pathological and immunohistochemical measurements from a biopsy of the hepatic metastasis. A literature review identified only four similar cases had been reported. Despite being rare and having a poor prognosis, hormone-producing neuroendocrine tumors that derive from the gallbladder should be considered in the differential diagnosis of ectopic ACTH syndrome.

miR-452-5p suppressed the metastasis of Non-small cell lung cancer through regulating Moesin.

Background: Non-small cell lung cancer (NSCLC) is a common malignant tumor, and it is characterized by high mortality. MicroRNA-452-5p (miR-452-5p) and Moesin (MSN) have been proved to be related with regulation of tumors. If miR-452-5p could regulate NSCLC through targeting MSN remain unclear. Methods: TargetScan data and GEPIA databases were used to predict binding site and analyze gene expression, respectively. EdU staining, wound healing, and Transwell assays were performed to measure cell proliferation, migration, and invasion, respectively. Results: The binding site between miR-452-5p and MSN was predicted and validated. Overexpression of miR-452-5p cell lines were constructed, and miR-452-5p mimics markedly inhibited the migration, invasion, and proliferation ability of both H322 and A549 cells, but these effects of miR-452-5p were reversed by pcDNA-MSN. pcDNA-MSN significantly reversed the influence of miR-452-5p mimics on the EMT related proteins expression in H322 and A549 cell lines by decreasing E-cadherin and increasing N-cadherin. Significant higher expression of MSN in lung adenocarcinoma and lung squamous cell carcinoma was observed through GEPIA and TCGA data base analysis. Higher expression of MSN is positively correlated with advanced lung cancer and suggests poor prognosis. Conclusions: We demonstrated that miR-452-5p modulated the cell proliferation, migration, invasion, and EMT process of H322 and A549 cell lines through targeting MSN. This research might provide a novel prevention and treatment target for NSCLC.

A sector-disaggregated cross-regional emission analysis for carbon mitigation policies from production and consumption perspectives.

As one of the most challenging environment issues worldwide, climate change has posed a serious threat to habitat, species, and people's livelihoods. In this study, a sector-disaggregated cross-regional emission analysis model is developed to systematically analyze enviro-economic effects of sector-level carbon mitigation efforts from both production and consumption perspectives for supporting climate change-related policymaking. A special case study of Hubei Province, China, is conducted to demonstrate the potential benefits of its use in the climate change related policymaking field. The power generation sector has been disaggregated into five subsectors based on different power generation technologies to help investigate the potential of such technologies to carbon emission mitigations. The carbon mitigation policy scenarios from both industry optimization and demand substitute perspectives will further be explored to provide bases for decision makers to formulate the desired carbon mitigation policy aimed at different regions and sectors. Results indicate that dominant direct and indirect CO2 emissions in Hubei Province are from the Production and supply of fossil-fuel power sector and Construction sector, respectively. When industry optimization policies on the fossil-fuel power sector (in Hubei), there are significant effects on the CO2 emission mitigation whichever regions. Therefore, industry optimization policies are suggested for implementation in specific sectors with close intersectoral/interprovince trade contacts and significant emissions to achieve joint carbon emission mitigations.

TRIM9 Interacts with ZEB1 to Suppress Esophageal Cancer by Promoting ZEB1 Protein Degradation via the UPP Pathway.

Background: Esophageal cancer remains one of the most lethal malignant diseases globally. Previous studies indicated that TRIM9 (Tripartite Motif Containing 9) is a potential marker in breast cancer patients. Therefore, in the current research, we intended to clarify the regulatory network of TRIM9 and its relative role in esophageal cancer patients. We aimed to elucidate the regulatory role of TRIM9 in esophageal cancer. Methods: Clinical tumor tissue samples combined with cancer cell line models were utilized to explore the TRIM9 expression pattern. Functional experiments including transwell assay, cell viability assay, and ubiquitination blocking experiments were performed to evaluate the role of the TRIM9/ZEB1 (zinc finger E-box binding homeobox 1) axis and UPP pathway in esophageal cancer progression and exacerbation. Results: Both esophageal cancer samples and cell line models showed significantly suppressed levels of TRIM9. Functional experiments confirmed that TRIM9 overexpression inhibited the cell viability, invasiveness, and stem-like phenotype of cancer cells. Subsequent investigations suggested that TRIM9-ZEB1 interaction accelerated ZEB1 protein degradation through the modulation of the UPP pathway, which confirmed the protective role of TRIM9 in esophageal cancer progression and metastasis. Conclusion: This study concluded that TRIM9 was a tumor suppressor that interacted with ZEB1 and accelerated ZEB1 protein degradation via the ubiquitin-proteasome pathway (UPP). Our research emphasized TRIM9-ZEB1 interaction as a valuable target for esophageal cancer treatment in future development. More detailed studies are needed to further consolidate our findings.

bITH, a blood-based metric of intratumor heterogeneity, is associated with clinical response to immune checkpoint blockade in non-small cell lung cancer.

BACKGROUND: Intratumor heterogeneity (ITH) has been associated with poor prognosis in advanced non-small cell cancer (NSCLC) patients receiving immune checkpoint blockade (ICB) therapies. However, there is currently no evidence supporting an ITH metric as a predictor of clinical benefit from ICB. The unique advantages of blood make it a promising material for ITH estimation and relevant applications. This study aims to develop and validate a blood-based ITH index for predicting ICB response. METHODS: NSCLC patients from the OAK and POPLAR clinical trials were used as the training cohorts for algorithm development. Survival analyses with overall survival (OS) and progression-free survival (PFS) as endpoints were performed to assess clinical response. The predictive value of bITH was subsequently validated with an independent cohort of 42 NSCLC patients treated with PD-1 blockade. FINDINGS: bITH was significantly associated with the differential OS and PFS elicited by atezolizumab vs. docetaxel in both univariable and multivariable analyses in the OAK patients, suggesting bITH as an independent predictor for response to ICB. Moreover, compared with blood tumor mutation burden (bTMB), bITH enabled greater OS segregation and comparable PFS segregation, and obtained a predictive role regardless of bTMB status. Moreover, the association between bITH and PFS was validated with an independent cohort. INTERPRETATION: Patients with low blood-based ITH metric manifest significant OS and PFS benefit from immunotherapy versus chemotherapy. Future research is awaited to corroborate our findings and to enrich the clinical utility of ITH. FUNDING: This study was supported by the National Natural Science Foundation of China (Nos. 81972718 and 81572321), the Natural Scientific Foundation of Zhejiang Province, China (No. LY19H160007), the Science and Technology Program for Health and Medicine in Zhejiang Province, China (No. 2021KY541), the Scientific Research Project, Science and Technology Department of Sichuan Province (No. 21YYJC1616), the Scientific Research Project, Sichuan Medical Association (No. S20002), Wu Jieping Medical Foundation (No. 320.6750), and 2018 Entrepreneurial Leading Talent of Guangzhou Huangpu District and Guangzhou Development District (No. 2022-L023).

SIRT1 activation synergizes with FXR agonism in hepatoprotection via governing nucleocytoplasmic shuttling and degradation of FXR.

Farnesoid X receptor (FXR) is widely accepted as a promising target for various liver diseases; however, panels of ligands in drug development show limited clinical benefits, without a clear mechanism. Here, we reveal that acetylation initiates and orchestrates FXR nucleocytoplasmic shuttling and then enhances degradation by the cytosolic E3 ligase CHIP under conditions of liver injury, which represents the major culprit that limits the clinical benefits of FXR agonists against liver diseases. Upon inflammatory and apoptotic stimulation, enhanced FXR acetylation at K217, closed to the nuclear location signal, blocks its recognition by importin KPNA3, thereby preventing its nuclear import. Concomitantly, reduced phosphorylation at T442 within the nuclear export signals promotes its recognition by exportin CRM1, and thereby facilitating FXR export to the cytosol. Acetylation governs nucleocytoplasmic shuttling of FXR, resulting in enhanced cytosolic retention of FXR that is amenable to degradation by CHIP. SIRT1 activators reduce FXR acetylation and prevent its cytosolic degradation. More importantly, SIRT1 activators synergize with FXR agonists in combating acute and chronic liver injuries. In conclusion, these findings innovate a promising strategy to develop therapeutics against liver diseases by combining SIRT1 activators and FXR agonists.

MiR-942-5p inhibits tumor migration and invasion through targeting CST1 in esophageal squamous cell carcinoma.

INTRODUCTION: Cysteine Protease Inhibitor 1 (CST1), a cystatin superfamily protein with the effect on the inhibition of cysteine protease activity, is reported to be involved in the development of many malignancies. MiR-942-5p has been demonstrated its regulatory effects on some malignancies. However, the roles of CST1 and miR-942-5p on esophageal squamous cell carcinoma (ESCC) are still unknown up to now. METHODS: The expression of CST1 in ESCC tissues was analyzed by TCGA database, immunohistochemistry, and RT-qPCR, respectively. Matrigel-uncoated or-coated transwell assay was used to determine the effect of CST1 on migration and invasion of ESCC cells. Regulatory effect of miR-942-5p on CST1 was detected by dual luciferase assay. RESULTS: CST1 was ectopically highly expressed in ESCC tissues, and had the effect on promoting the migration and invasion of ESCC cells by upregulating phosphorylated levels of key effectors including MEK1/2, ERK1/2, and CREB in MEK/ERK/CREB pathway. Dual-luciferase assay results showed that miR-942-5p had a regulatory effect on targeting CST1. CONCLUSIONS: CST1 plays a carcinogenic role on ESCC, and miR-942-5p can regulate the migration and invasion of ESCC cells by targeting CST1 to downregulate MEK/ERK/CREB signaling pathway, suggesting that miR-942-5p/CST1 axis might be a promising target for diagnosis and treatment of ESCC.

Failure to achieve reduction on developmental dysplasia of hip: an ultrasound evaluation.

BACKGROUND: Ultrasound examination of the medial side of the hip joint has been rarely used to evaluate the status of developmental dysplasia of the hip (DDH) in Pavlik harness treatment according to the literature. PURPOSE: To analyze the effects of cartilaginous acetabulum, hip joint labrum, and acetabular tissue on the reduction of DDH. MATERIAL AND METHODS: A total of 50 cases (100 hips) were detected by the Graf method with a high-frequency linear transducer (L 5-12), and there were 59 dislocated hips and 41 non-dislocated hips. Patients were treated with a Pavlik harness. Ultrasound examination of the medial side of the hip joint was performed for follow-up. The hip joints were divided into three groups: the non-dislocated group; the reducible group; and the non-reducible group. RESULTS: The success rate of reduction was significantly higher when the acetabulum cartilage was located on the cephalic side (chi-square = 28.12, P < 0.001). The success rate was also significantly higher when the hip joint labrum was located on the cephalic side (chi-square = 17.21, P < 0.001). Type III and D had a higher success rate of reduction than type IV (P < 0.001). The pairwise comparison of the measurements of acetabular tissue between the non-dislocated group, the reducible group, and the non-reducible group showed statistical differences (P < 0.001). CONCLUSION: The present study confirmed that the location of acetabulum cartilage and hip joint labrum affected the outcome of treatment. The degree of dislocation and the amount of acetabular tissue were correlated with the success rate of treatment.

USP2 Inhibits Lung Cancer Pathogenesis by Reducing ARID2 Protein Degradation via Ubiquitination.

Background: Ubiquitination is an important regulator in physiological and pathological conditions. Ubiquitin-specific protease 2 (USP2), as a member of the USP family, exhibits oncogenic effects in multiple malignancies. However, the exact role of USP2 has not been well clarified in lung cancer pathogenesis and progression. Therefore, we aimed to further investigate the regulatory roles of USP2 in lung cancer in this study. Methods: Firstly, immunoprecipitation-Mass Spectrometry (IP-MS), Co-immunoprecipitation (Co-IP), combined with immunofluorescent colocalization method, was conducted for USP2 protein interaction analysis in lung cancer cell lines. qRT-PCR, Western blot, and immunohistochemistry assays explored the USP2 expression pattern and USP2/ARID2- (AT-rich interactive domain 2-) specific shRNAs and overexpression vectors. Co-IP assays were designed to validate USP2-ARID2 protein interaction. Further functional studies including CHX chase assay, transwell assay, and wound healing assay were subsequently applied to evaluate the impact of USP2 modulation on lung cancer cells. Results: USP2 suppression was characteristic in lung cancer cell line models and lung cancer samples. USP2 and ARID2 demonstrated protein-protein interaction and overlapping localization in cancer cell models. Functional experiments suggested USP2 inhibited lung cancer cell invasion and migration by reducing ARID2 protein degradation. Subsequent ubiquitination assays indicated ARID2 protein degradation via the ubiquitination was significantly reduced by USP2 interaction. Conclusions: Our study provided novel insight that USP2 might suppress lung cancer by reducing ARID2 protein degradation via ubiquitination.

Development and validation of short-term renal prognosis prediction model in diabetic patients with acute kidney injury.

OBJECTIVE: Diabetes is a major cause of the progression of acute kidney injury (AKI). Few prediction models have been developed to predict the renal prognosis in diabetic patients with AKI so far. The aim of this study was to develop and validate a predictive model to identify high-risk individuals with non-recovery of renal function at 90 days in diabetic patients with AKI. METHODS: Demographic data and related laboratory indicators of diabetic patients with AKI in the First Affiliated Hospital of Guangxi Medical University from January 31, 2012 to January 31, 2022 were retrospectively analysed, and patients were followed up to 90 days after AKI diagnosis. Based on the results of Logistic regression, a model predicting the risk of non-recovery of renal function at 90 days in diabetic patients with AKI was developed and internal validated. Consistency index (C-index), calibration curve, and decision curve analysis were used to evaluate the differentiation, accuracy, and clinical utility of the prediction model, respectively. RESULTS: A total of 916 diabetic patients with AKI were enrolled, with a male to female ratio of 2.14:1. The rate of non-recovery of renal function at 90 days was 66.8% (612/916). There were 641 in development cohort and 275 in validation cohort (ration of 7:3). In the development cohort, a prediction model was developed based on the results of Logistic regression analysis. The variables included in the model were: diabetes duration (OR = 1.022, 95% CI 1.012-1.032), hypertension (OR = 1.574, 95% CI 1.043-2.377), chronic kidney disease (OR = 2.241, 95% CI 1.399-3.591), platelet (OR = 0.997, 95% CI 0.995-1.000), 25-hydroxyvitamin D3 (OR = 0.966, 95% CI 0.956-0.976), postprandial blood glucose (OR = 1.104, 95% CI 1.032-1.181), discharged serum creatinine (OR = 1.003, 95% CI 1.001-1.005). The C-indices of the prediction model were 0.807 (95% CI 0.738-0.875) and 0.803 (95% CI 0.713-0.893) in the development and validation cohorts, respectively. The calibration curves were all close to the straight line with slope 1. The decision curve analysis showed that in a wide range of threshold probabilities. CONCLUSION: A prediction model was developed to help predict short-term renal prognosis of diabetic patients with AKI, which has been verified to have good differentiation, calibration degree and clinical practicability.

The Diagnostic Value of Bedside Echocardiography and Lower Extremity Blood Vessels in Acute Pulmonary Embolism.

Objective: The study aimed to evaluate the value of bedside echocardiography (TTE) and lower extremity blood vessels in diagnosis and prognosis of acute pulmonary embolism (APE). Methods: A retrospective study was performed on 53 patients with APE diagnosed by CT pulmonary angiography (CTPA) (systemic systolic blood pressure was >90 mmHg at time of consultation, and systemic systolic blood pressure decreased by <40 mmHg compared with basic value in those with hypertension). All patients underwent TTE examination before treatment. The high-risk factors, clinical manifestations, laboratory tests, and prognosis were retrospectively analyzed. Results: The rate of PE-related deterioration (cardiopulmonary resuscitation, tracheal intubation, cardiogenic shock, and death) within 14 days of hospitalization in RVD was 28%, and mortality rate (sudden death) was 20%, compared with non-RVD (both 0%). TTE examination showed that RVD as a predictor of pulmonary embolism-related death had a sensitivity of 100%, a specificity of 58%, a positive predictive value of 20%, and a negative predictive value of 100%. Conclusions: (1) TTE has increasingly shown obvious advantages in diagnosis of APE. It can detect direct or indirect signs of pulmonary embolism, confirm diagnosis or suspected diagnosis, and noninvasively and dynamically observe hemodynamic changes of heart in patients with acute PTE before and after treatment.. (2) The PE-related exacerbation rate (28%) or mortality (20%) of APE patients in normotensive with RVD was higher without RVD (0%). RVD is an independent predictor of poor prognosis in normotensive acute PTE. TTE tests allow people to identify people at risk of early death. The short-term prognosis of patients without RVD was better (14 days).

Fucosylated exosomal miRNAs as promising biomarkers for the diagnosis of early lung adenocarcinoma.

Background: Considering the absence of apparent symptoms at the early stage, most patients with lung adenocarcinoma (LUAD) present at an advanced stage, leading to a dismal 5-year survival rate of <20%. Thus, finding perspective non-invasive biomarkers for early LUAD is very essential. Methods: We developed a fucose-captured strategy based on lentil lectin-magnetic beads to isolate fucosylated exosomes from serum. Then, a prospective study was conducted to define the diagnostic value of serum exosomal miRNAs for early LUAD. A total of 310 participants were enrolled, including 146 LUAD, 98 benign pulmonary nodules (BPNs), and 66 healthy controls (HCs). Firstly, exosome miRNAs in the discovery cohort (n = 24) were profiled by small RNA sequencing. Secondly, 12 differentially expressed miRNAs (DEmiRs) were selected for further screening in a screening cohort (n = 64) by qRT-PCR. Finally, four candidate miRNAs were selected for further validation in a validating cohort (n = 222). Results: This study demonstrated the feasibility of a fucose-captured strategy for the isolation of fucosylated exosomes from serum, evidenced with exosomal characteristics identified by transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and Western blotting, as well as rapid and convenient operation of <10 min. Furthermore, a miRNA panel for early LUAD composed of miR4732-5p, miR451a, miR486-5p, and miR139-3p was defined with an AUC of 0.8554 at 91.07% sensitivity and 66.36% specificity. Conclusions: The fucose-captured strategy provides a reliable, as well as rapid and convenient, approach for the isolation of tumor-derived exosomes from serum. A four-fucosylated exosomal miRNA panel presents good performance for early LUAD diagnosis.