Tripartite motif containing 59 (TRIM59) promotes esophageal cancer progression via promoting MST4 expression and ERK pathway.

Objective: To detect the expression of tripartite motif containing 59 (TRIM59) in human esophageal cancer (EC) tissues and explore whether TRIM59 could affect the progression of EC.Methods: Quantitative PCR and immunohistochemistry assays were performed to detect the expression of TRIM59 in 40 human EC tissues and corresponding non-tumor tissues. The correlations between TRIM59 expression and clinical pathological features of patients with EC were also investigated. CCK-8, colony formation, wound closure, and transwell assays were performed to detect the effects of TRIM59 on EC cells in vitro., Immunoblotting assays were performed to detect the effects of TRIM59 on the expression of mammalian sterile-20-like kinase 4 (MST4) and ERK pathway.Results: We reported increased expression of TRIM59 in human EC tissues, and its expression was correlated with clinical features, including metastasis (p = .011*) and maximum diameter (p = .027*), in patients with EC. We further found that TRIM59 contributed to the proliferation and invasion of EC cells via regulating mammalian sterile-20-like kinase 4 (MST4) expression and ERK pathway.Conclusion: Our data confirmed the involvement of TRIM59 in EC progression and proposed that TRIM59 could serve as a promising therapeutic target for the treatment of EC.

The Depletion of ABI3BP by MicroRNA-183 Promotes the Development of Esophageal Carcinoma.

BACKGROUND: Esophageal cancer (EC), as a serious threat to human life and health, is one of the most common cancers around the world. Many studies have suggested that many microRNAs are involved in tumorigenesis and progression. METHODS: To search for a novel and promising predictive therapeutic target or biomarker to achieve the goal of the early diagnosis and treatment of EC, we used the EC cell lines Eca-109 and KYSE-150 and normal human esophageal epithelial cells (HEECs) to investigate the effect of ABI3BP on EC. RESULTS: We found that ABI family member 3 binding protein (ABI3BP) was downregulated in EC and suppressed the proliferation, activity, migration, and invasion of EC cells. ABI3BP was downregulated by miR-183, which plays the role of an oncogene. CONCLUSION: ABI3BP and miR-183 can be considered potential biomarkers for the diagnosis of patients with EC and can be effective targets for antitumor therapy.

MiR-129-5p inhibits non-small cell lung cancer cell stemness and chemoresistance through targeting DLK1.

Non-small cell lung cancer (NSCLC) stemness and chemoresistance represent significant barriers to successful treatment. Downregulation of microRNA 129 (miR-129) has been implicated in a variety of cancers, and miR-129-5p has recently been shown to reduce lung cancer proliferation and metastasis. In this study, we used NSCLC cell lines A549 and H460 to investigate the effects of miR-129-5p on NSCLC stemness and chemoresistance. CD133 + stem cells in both lines showed reduced miR-129-5p expression, and introducing miR-129-5p into these cells reduced stem cell markers and self-renewal ability, as measured by qRT-PCR, western blot, MTT assays, and sphere formation assays. MTT, colony formation, and DAPI staining assays further revealed that miR-129-5p inhibits NSCLC chemoresistance when the cells are treated with varying doses of CDDP. The target prediction algorithm TargetScan allowed us to identify notch signaling receptor delta-like 1 homolog (DLK1) as a potential target for miR-129-5p in its inhibition of NSCLC stemness and chemoresistance. Indeed, our DLK1 luciferase reporter plasmid demonstrated that miR-129-5p reduces DLK1 expression. Furthermore, DLK1 overexpression partially rescued inhibition of NSCLC stemness and chemoresistance caused by miR-129-5p. Overall, these results demonstrate that miR-129-5p inhibits NSCLC stemness and chemoresistance through direct targeting of DLK1. They suggest that miR-129-5p and DLK1 can play a role in an effective treatment strategy for NSCLC.

Progress in the treatment of esophageal neuroendocrine carcinoma.

Esophageal neuroendocrine neoplasms are rare. With the improvement and popularization of diagnostic methods, the morbidity statistics have increased annually in recent years. There are currently no treatment guidelines for esophageal neuroendocrine neoplasms, and surgery is the only cure. This usually involves radical surgery when the tumor is limited to the primary site or when only regional lymph node metastasis occurs. Surgical treatment is key to treating esophageal neuroendocrine neoplasms, but combined treatment with chemotherapy and radiotherapy can significantly improve patient survival. The effect of radiotherapy alone on this disease is poor. However, targeted endocrine therapy can improve endocrine hormone symptoms. The prognosis of patients with esophageal neuroendocrine neoplasms is mainly determined by the pathological stage. With the development of molecular biology techniques, the combination of targeted drugs and traditional chemotherapy is expected to provide novel ideas and directions for the treatment of esophageal neuroendocrine neoplasms in the coming years. In this article, the status of esophageal neuroendocrine tumor treatments was reviewed in detail.

The Effect of Immunonutrition on the Postoperative Complications in Thymoma with Myasthenia Gravis.

Object. To test whether preoperative immunonutrition is efficacious in reducing postoperative complications in patients of thymoma with myasthenia gravis (MG). Material and Methods. A total of 244 patients operated on for thymoma with myasthenia gravis were prospectively assigned to two groups, each receiving seven-day preoperative and seven-day postoperative nutrition. The patients in immunonutrition group were given oral immunonutrition (IN). The patients in control group received oral standard nutrition. Immunonutritional and inflammatory biomarkers (IgA, IgG, IgM, CD3t, CD4t, CD8t, CD4t/CD8t ratio, NK-cell, prealbumin, albumin, white blood cells counts, and C-reactive protein) and clinical variables (age, gender, BMI, performance status, type of thymoma, type of MG, operative time, pathology, operative approach, postoperative complications, quantity of drainage, hospital stays) were examined. Results. A significant reduction in the length of hospital stay, quantity of drainage, and postoperative complications was observed in the IN group (p < 0.05). An increase in the level of IgA, IgG, IgM, CD3+T, CD4+T, CD4+T/CD8+T, WBC, CRP, and NK-cell in the IN group was observed after thymectomy, while a decrease was seen with regard to prealbumin and albumin (p < 0.05). Conclusion. Preoperative immunonutrition support is effective in reducing postoperative complications in patients of thymoma with MG. It helps to lower the risk of postoperative infectious complications and hospital stays.

[Efficacy of adjuvant therapy in 110 patients with N1 lymph node metastasis of esophageal squamous cell carcinoma].

OBJECTIVE: The aim of this study was to evaluate the effect of postoperative adjuvant therapy on the survival in patients with N1 lymph node metastasis of esophageal squamous cell carcinoma (ESCC). METHODS: 110 patients with positive N1 lymph node metastasis of esophageal squamous carcinoma were included in this study. The surgery group included 46 cases and the postoperative adjuvant therapy group included 64 cases (24 cases in the adjuvant chemotherapy subgroup and 40 cases in the adjuvant concurrent chemoradiotherapy). The disease-free survival (DFS) and overall survival (OS) of the two groups were compared and the prognostic factors were analyzed by multivariate Cox model. RESULTS: In the postoperative adjuvant therapy group, the DFS (16.8 months) and OS (21.3 months) were significantly prolonged compared with those in the surgery group (10.6 months, P=0.007) and (13.7 months, P=0.001), respectively. Postoperative adjuvant chemotherapy significantly extended the OS (31.1 months) of N1-positive patients compared with 13.7 months (P=0.002) in the surgery group. But there were no significant differences between the DFS in the two subgroups (16.3 and 16.8 months, P=0.346) and between the OS (23.4 and 21.3 months, P=0.491). Postoperative adjuvant therapy was an independent prognostic factor in the ESCC patients with N1 lymph node metastasis. CONCLUSION: Postoperative adjuvant therapy can improve the prognosis and prolong the survival time in ESCC patients with positive N1 lymph node metastasis.

NADPH oxidase 1-dependent ROS is crucial for TLR4 signaling to promote tumor metastasis of non-small cell lung cancer.

Recent evidence demonstrated an enhanced metastasis of non-small cell lung cancer (NSCLC) cells induced by lipopolysaccharide (LPS) stimulation, which reflected an important role of inflammation in tumor progression. However, the underlying mechanisms still remain unclear. Here, we evaluated the potential role of reactive oxygen species (ROS) in Toll-like receptor 4 (TLR4) signaling enhanced NSCLC metastasis. NSCLC cells were isolated from clinical surgical tissues. We found that LPS stimulation of NSCLC cells facilitates their metastasis that was accompanied by increased ROS production and could be abrogated by ROS inhibition. NADPH oxidase was essential for TLR4 signaling-enhanced NSCLC metastasis. Elevated NADPH oxidase 1 (NOX1) expression by LPS stimulation was observed. Blockade of NOX1 with ML171 alleviated enhanced NSCLC metastasis by TLR4 signaling. Enforced NOX1 expression promoted TLR4 signaling-enhanced NSCLC metastasis, while decreased NOX1 expression inhibited TLR4 signaling-enhanced NSCLC metastasis. Further, NOX1 could regulate the expression of CXCR4 and matrix metallopeptidase 9 (MMP9) in NSCLC cells. NOX1 expression in tumor tissues was correlated with TLR4 expression and clinical stages in NSCLC patients. Finally, inhibition of NOX1/ROS prevented enhanced lung tumor burdens of NSCLC by LPS-induced acute lung infection. Our findings demonstrated a crucial role of NOX1-dependent ROS for TLR4 signaling to enhance the metastasis of NSCLC, which could further the understanding of NSCLC pathogenesis and helpful for developing novel therapeutics for NSCLC.

Circulating cell-free DNA-based methylation pattern in plasma for early diagnosis of esophagus cancer.

With the increased awareness of early tumor detection, the importance of detecting and diagnosing esophageal cancer in its early stages has been underscored. Studies have consistently demonstrated the crucial role of methylation levels in circulating cell-free DNA (cfDNA) in identifying and diagnosing early-stage cancer. cfDNA methylation pertains to the methylation state within the genomic scope of cfDNA and is strongly associated with cancer development and progression. Several research teams have delved into the potential application of cfDNA methylation in identifying early-stage esophageal cancer and have achieved promising outcomes. Recent research supports the high sensitivity and specificity of cfDNA methylation in early esophageal cancer diagnosis, providing a more accurate and efficient approach for early detection and improved clinical management. Accordingly, this review aims to present an overview of methylation-based cfDNA research with a focus on the latest developments in the early detection of esophageal cancer. Additionally, this review summarizes advanced analytical technologies for cfDNA methylation that have significantly benefited from recent advancements in separation and detection techniques, such as methylated DNA immunoprecipitation sequencing (MeDIP-seq). Recent findings suggest that biomarkers based on cfDNA methylation may soon find successful applications in the early detection of esophageal cancer. However, large-scale prospective clinical trials are required to identify the potential of these biomarkers.

Atrial arrhythmias after pulmonary resection: the important role of pulmonary vein resection.

BACKGROUND: Atrial arrhythmias (AAs) remain one of the most common complications after pulmonary resection. The association between postoperative AAs and pulmonary vein (PV) resection has not previously been clearly elucidated. A retrospective study on this issue is reported. METHODS: A total of 125 patients were involved in this study and all the performed surgical procedures and all postoperative AAs were carefully reviewed and recorded. A univariate and multivariate analyses were utilized to clarify the effect of PV resection on postoperative AAs. RESULTS: The overall incidence of postoperative AAs was 14.4% (n = 18). A stepwise increase in the incidence of AAs was observed from none, to the inferior of PV resection only, superior PV resection only and up to both inferior and superior PV resection (0, 3.1, 14.3, and 38.5%, respectively; p = 0.000). During multivariate analysis, PV resection was identified as an independent risk factor for postoperative AAs when it was entered either as an ordinal or as a categorical variable. The area under the receiver operating characteristic curve of PV resection revealed 0.786 (95% confidence interval [CI], 0.685-0.887), which was significantly larger than the extent of pulmonary resection (0.724; 95% CI, 0.637-0.800; p = 0.015). CONCLUSION: PV resection plays an important role in the development of postoperative AAs after pulmonary resection and could be used as a good predictor for postoperative AAs.

Clinical therapeutic effects and prognosis of video-assisted thoracoscopic surgery-guided pulmonary lobectomy combined with mediastinal lymph node dissection in lung carcinoma.

We investigated the clinical therapeutic effects and prognosis of video-assisted thoracoscopic surgery (VATS) in mediastinal lymph node dissection of lung carcinoma. A total of 312 patients were divided into high-risk and conventional risk groups according to the severity of the disease. High-risk group (n=137) received thoracoscope-guided anatomical pulmonary segmentectomy and systematic lymph node dissection as well as conventional risk group (n=175) received thoracoscope-guided pulmonary lobectomy and systematic lymph node dissection. The results revealed that there are significant differences in age, gender, location, lymph node resection methods, and histological classification in the two groups (P<0.05). Moreover, in comparison with the high-risk group, T stage was higher in the conventional group and showed significant statistical significance (P<0.01). The analysis of independent risk factors of the above differences showed that T staging and histological classification showed high-risk coefficients for lymph node dissection. The risk coefficient was increased with patients' age. The 5-year survival rate, disease-free survival, and postoperative recurrence rate of the patients in the two groups all indicated no obvious statistical differences. Consequently, thoracoscope-guided lymph node dissection could enhance the detection rate of lymph node metastasis. For the adenocarcinoma (AD) patients with T staging greater than T1, lymph node dissection could provide more accurate pathological staging. Anatomical pulmonary segmentectomy combined with systematic lymph node dissection should be applied in the treatment of elderly, high-risk, and advanced stage (prothrombin time (PT) state >2 cm, ≤3 cm) patients with non-small cell lung carcinoma (NSCLC). Taken together,thoracoscope-guided lymph node dissection could improve the detection rate of lymph node metastasis. In this case, the complete resection of lesions could be ensured. Besides, normal pulmonary tissues were preserved to the maximum extent with minimal trauma, safety, fast postoperative recovery, and definite long-term therapeutic effects.

Combined RNAi targeting human Stat3 and ADAM9 as gene therapy for non-small cell lung cancer.

[This retracts the article DOI: 10.3892/ol.2015.4018.].

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.

Analysis of pulmonary artery variation based on 3D reconstruction of CT angiography.

Objective: The aim of this study is to acquire pulmonary CT (Computed tomography) angiographic data for the purpose of creating a three-dimensional reconstruction. Additionally, we aim to analyze the features and deviations of the branches in both pulmonary lobes. This information is intended to serve as a more comprehensive and detailed reference for medical professionals when conducting preoperative evaluations and devising surgical plans. Method: Between August 2019 and December 2021, 420 patients were selected from the thoracic surgery department at the First Hospital of Jilin University, and underwent pulmonary 64 channel contrast enhanced CT examinations (Philips ICT 256). The images were acquired at a 1.5 mm slice thickness, and the DCM files that complied with DICOM (Digital Imaging and Communications in Medicine) standards were analysed for 3D (three dimensional) reconstruction using Mimics 22.0 software. The reconstructed pulmonary artery models were assessed by attending chest surgeons and radiologists with over 10 years of clinical experience. The two-dimensional image planes, as well as the coronary and sagittal planes, were utilized to evaluate the arteries. The study analyzed the characteristics and variations of the branches and courses of pulmonary arteries in each lobe of the lungs, with the exception of the subsegmental arterial system. Two chest surgeons and two radiologists with professional titles-all of whom had over a decade of clinical experience-jointly evaluated the 3D models of the pulmonary artery and similarly assessed the characteristics and variations of the branches and courses in each lobe of the lungs. Results: Significant variations were observed in the left superior pulmonary artery across the 420 subjects studied. In the left upper lobe, the blood supply of 4 arteries accounted for 50.5% (n = 212), while the blood supply of 2 arteries in the left lower lobe was the most common, accounting for 79.5% (n = 334). The greatest variation in the right pulmonary artery was observed in the branch supply of the right upper lobe mediastinal artery. In the majority of cases (77.9%), there were two arteries present, which was the most common configuration observed accounting for 64% (n = 269). In the right inferior lobe of the lung, there were typically 2-4 arteries, with 2 arteries being the most common configuration (observed in 79% of cases, n = 332). Conclusion: The three-dimensional reconstruction of pulmonary artery CT angiography enables clear observation of the branches and distribution of the pulmonary artery while also highlighting any variations. This technique holds significant clinical value for preoperative assessments regarding lesions and blood vessels.

Nomogram model combined thrombelastography for venous thromboembolism risk in patients undergoing lung cancer surgery.

Background: The aim of this study was to develop a nomogram model in combination with thromboelastography (TEG) to predict the development of venous thromboembolism (VTE) after lung cancer surgery. Methods: The data of 502 patients who underwent surgical treatment for lung cancer from December 2020 to December 2022 were retrospectively analyzed. Patients were then randomized into training and validation groups. Univariate and multivariate logistic regression analyses were carried out in the training group and independent risk factors were included in the nomogram to construct risk prediction models. The predictive capability of the model was assessed by the consistency index (C-index), receiver operating characteristic curves (ROC), the calibration plot and decision curve analysis (DCA). Results: The nomogram risk prediction model comprised of the following five independent risk factors: age, operation time, forced expiratory volume in one second and postoperative TEG parameters k value(K) and reaction time(R). The nomogram model demonstrated better predictive power than the modified Caprini model, with the C-index being greater. The calibration curve verified the consistency of nomogram between the two groups. Furthermore, DCA demonstrated the clinical value and potential for practical application of the nomogram. Conclusion: This study is the first to combine TEG and clinical risk factors to construct a nomogram to predict the occurrence of VTE in patients after lung cancer surgery. This model provides a simple and user-friendly method to assess the probability of VTE in postoperative lung cancer patients, enabling clinicians to develop individualized preventive anticoagulation strategies to reduce the incidence of such complications.

Case report: Lung transplantation for treatment of paraquat intoxication: timing of transplantation.

Objective: To analyze the optimal timing of lung transplantation and summarize postoperative complications and their management after paraquat poisoning. Methods: Here, we present the clinical course of a 17-year-old boy with paraquat poisoning, in whom bilateral lung transplantation (LT) was performed. We reviewed the eight previously published articles relevant to LT after paraquat poisoning to summarize the therapeutic strategy. Results: A 17-year-old boy was admitted to the hospital after ingestion of 30-50 mL 25% paraquat. Mechanical ventilation was initiated on the 25th day after intoxication. Venovenous extracorporeal membrane oxygenation was initiated on the 26th day. Sequential bilateral LT was performed on the 27th day. Several complex postoperative complications occurred and the patient was discharged on the 50th day postoperatively. Eight case reports were included in the literature review, including 11 patients with paraquat poisoning undergoing LT. Three patients died due to paraquat poisoning leading to fibrosis in the transplanted lungs or postoperative complications. Eight patients survived during follow-up. Conclusion: LT after herbicide poisoning should be planned when hepatorenal function starts to recover, and waiting for complete recovery is unnecessary. Prevention of infection before surgery is important to reduce the incidence of postoperative infection. Complex perioperative complications caused by the herbicide itself or the late timing of transplantation can be successfully managed by a multidisciplinary team.

FSCN1 Promotes Esophageal Carcinoma Progression Through Downregulating PTK6 via its RNA-Binding Protein Effect.

Objective: Esophageal squamous cell carcinoma (ESCC) causes many deaths worldwide every year. Fascin actin-bundling protein 1(FSCN1) has been reported to be a promoter of ESCC via its actin-binding function, however, its new role as an RNA-binding protein (RBP) has not been investigated. Here, we explored the RBP role of FSCN1 in the development of ESCC. Methods: Whole-genome expression sequencing was performed to screen for altered genes after FSCN1 knockdown. RNA immunoprecipitation was performed to determine the target mRNA of FSCN1 as an RBP. In vitro experiments with ECA-109 and KYSE-150 and ex vivo experiments in tumor-bearing mice were performed to investigate the effects of FSCN1 and Protein Tyrosine Kinase 6 (PTK6) on ESCC progression. Results: FSCN1 could downregulate mRNA and the protein level of PTK6. The binding position of PTK6 (PTK6-T2) pre-mRNA to FSCN1 was determined. PTK6-T2 blocked the binding between FSCN1 and the pre-mRNA of PTK6, and thus reversed the promotion effect of FSCN1 on ESCC tumor progression via the AKT/GSK3ß signaling pathway. Conclusion: A novel effect of FSCN1, RBP-binding with the pre-mRNA of PTK6, was confirmed to play an important role in ESCC progression. PTK6-T2, which is a specific inhibitor of FSCN1 binding to the pre-mRNA of PTK6, could impede the development of ESCC.

[Retracted] Decreased microRNA­132 and its function in human non­small cell lung cancer.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the data shown in Fig. 5 and 6 were the same as those featured in another paper by different authors. Owing to the fact that the contentious data in the above article were already under consideration for publication elsewhere prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 11: 3601­3608, 2015; DOI: 10.3892/mmr.2015.3222].

Nanomedicine-Based Therapeutics to Combat Acute Lung Injury.

Acute lung injury (ALI) or its aggravated stage acute respiratory distress syndrome (ARDS) may lead to a life-threatening form of respiratory failure, resulting in high mortality of up to 30-40% in most studies. Although there have been decades of research since ALI was first described in 1967, the clinical therapeutic alternatives for ALI are still in a state of limited availability. Supportive treatment and mechanical ventilation still have priority. Despite some preclinical studies demonstrating the benefit of pharmacological interventions, none of these has been proved completely effective to date. Recent advances in nanotechnology may shed new light on the pharmacotherapy of ALI. Nanomedicine possesses targeting and synergistic therapeutic capability, thus boosting pharmaceutical efficacy and mitigating the side effects. Currently, a variety of nanomedicine with diverse frameworks and functional groups have been elaborately developed, in accordance with their lung targeting ability and the pathophysiology of ALI. The in-depth review of the current literature reveals that liposomes, polymers, inorganic materials, cell membranes, platelets, and other nanomedicine approaches have conferred attractive therapeutic benefits for ALI treatment. In this review, we explore the recent progress in the study of the nanomedicine-based therapy of ALI, presenting various nanomedical approaches, drug choices, therapeutic strategies, and outcomes, thereby providing insight into the trends.

Novel treatment for chylothorax after esophagectomy with 50% glucose pleurodesis.

Chylothorax is characterized by the presence of chyle in the pleural space and cardiothoracic surgery accounts for nearly half of all the cases. Treatment of chylothorax has traditionally been nonoperative, with alternative medical therapies involving the administration of octreotide or pleurodesis. Pleurodesis with chemical agents has previously been reported, but never with 50% glucose and 0.1% xylocaine. Herein, we report a successful method of intrapleural instillation of 50% glucose and 0.1% xylocaine to treat chylothorax. Five patients treated with this method were all recovered rapidly. This method can generate extensive adherence and prevent the effusion of the chylous fluid with minor side effects.

Long non-coding RNA DLEU2 promotes the progression of esophageal cancer through miR-30e-5p/E2F7 axis.

BACKGROUND: Emerging evidences have proven the important roles of lncRNAs in tumorigenesis and cancer biology. However, the function of lncRNA DLEU2 in the progression of esophageal cancer (EC) has not been elaborated. In the present study, we aimed to investigate the effects of lncRNA DLEU2 on the progression of EC and the underlying mechanism. METHODS: In this study, lncRNA DLEU2 was silenced by siRNA interference in EC cell lines Eca-109 and KYSE-150, and its expression was up-regulated in TE-1 cells by transfection with pcDNA3.1-DLEU2, and its biological functions were examined. Then, bioinformatics analysis and dual-luciferase reporter assay were used to identify the binding miRNA of lncRNA DLEU2 and the target gene of miRNA. In addition, loss-of-function assays were performed to detect the biological functions of the target gene. At last, the rescue assays were used to investigate the relationship among lncRNA DLEU2, miRNA and target gene. RESULTS: With the help of GEPIA analysis, we observed that lncRNA DLEU2 was up-regulated in EC tissues and associated with poor prognosis. Loss-of-function assay showed that silencing lncRNA DLEU2 inhibited the proliferation, migration and invasion of EC cells, and induced apoptosis by regulating the Bcl-2/Bax axis and Caspase cascade. Overexpression of lncRNA DLEU2 increased the proliferation, migration and invasion abilities of TE-1 cells, as well as decreased cell apoptosis. Bioinformatics analysis and dual-luciferase reporter assay verified that miR-30e-5p could directly bind with lncRNA DLEU2, and E2F7 was a direct target for miR-30e-5p in EC cells. Moreover, our data revealed that silencing E2F7 decreased the proliferation, migration and invasion abilities of EC cells, and induced apoptosis. Furthermore, the rescue assays demonstrated that the effects of lncRNA DLEU2 on the proliferation, migration and invasion of EC cells were reversed by miR-30e-5p inhibitor or up-regulation of E2F7. CONCLUSIONS: Our findings revealed the pro-oncogenic role of lncRNA DLEU2 and E2F7 in the progression of EC, suggesting that lncRNA DLEU2 exerts ceRNA functions in EC through regulating miR-30e-5p/E2F7 axis.