INTRODUCTION:Radiotherapy remains a cornerstone of treatment for non-small cell lung cancer (NSCLC). Despite its critical role, the emergence of radiation resistance remains a significant hurdle, often leading to therapeutic failure and disease progression. This research aimed to investigate the expression of Pellino E3 ubiquitin protein ligase family member 3 (PELI3) in NSCLC and examine its involvement in modulating the tumor's response to radiation. MATERIALS AND METHODS:To quantify PELI3 levels in NSCLC tissues, real-time PCR and Western blotting techniques were employed. The effects of silencing PELI3 on cancer cell proliferation were evaluated using CCK-8 and colony formation assays. Furthermore, an in vivo mouse xenograft model was used to corroborate the in vitro results. RESULTS:PELI3 expression was markedly elevated in NSCLC tumor samples relative to normal tissues and showed a strong association with clinical features, such as tumor volume, lymph node involvement, and radiotherapy responsiveness. Further analysis revealed that PELI3 promoted epithelial-to-mesenchymal transition (EMT) following radiation exposure. Suppressing PELI3 expression mitigated radiation-induced EMT in both cellular and animal models. DISCUSSION:Elevated PELI3 promotes radiation-induced EMT and radioresistance in NSCLC. Suppressing PELI3 reverses EMT features and enhances radiosensitivity in vitro and in vivo, highlighting PELI3 as a potential biomarker and therapeutic target to improve radiotherapy outcomes. CONCLUSION:These findings suggest that PELI3 could serve as a valuable prognostic marker in NSCLC and may represent a promising target to improve tumor sensitivity to radiotherapy.

IntroductionTumor necrosis factor receptor 1-associated death domain protein (TRADD) can trigger proapoptotic autophagy in non-small cell lung cancer (NSCLC). While the potential ubiquitin-protein ligase (E3) against TRADD is not well deciphered.MethodsUbiBrowser was used to predict the potential E3 ubiquitin ligase to bind with TRADD. Co-immunoprecipitation was performed in HEK293T cells co-transfected with Myc-PELI3, Flag-TRADD, or HA-Ub plasmids. Increasing doses of Myc-PELI3 were transfected into HCC827 and A549 cells, and the relative expression of TRADD was detected. Cycloheximide chase assay was performed in A549 cells transfected with Myc-PELI3 plasmids, and the stability of TRADD was revealed. CCK-8 assay was performed in A549 and HCC827 cells incubated with increasing doses of Mebendazole. The expression of TRADD and PELI3 after Mebendazole incubation was assayed with Western Blot and RT-PCR. The potential E3 ubiquitin ligase of PELI3 was predicted by the UbiBrowser platform, and the binding of PELI3 with TRADD was testified in HEK293T cells co-transfected with Myc-PELI3 and Flag-TRADD plasmids.ResultsPELI3 overexpression diminished the relative protein expression of TRADD, while not affecting the relative mRNA expression in both A549 and HCC827 cells. Cycloheximide assay and following HA-Ub detection demonstrated that PELI3 decreased the protein stability of TRADD by inducing polyubiquitination. Mebendazole inhibited the viability of HCC827 and A549 cells with diminished expression of PELI3 and increased expression of TRADD.ConclusionsPELI3 can function as an E3 ubiquitin ligase to ubiquitinate TRADD, and Mebendazole might be a promising drug to affect PELI3 expression in NSCLC.

Immune checkpoint inhibitors (ICIs), particularly PD-1/PD-L1 blockade, represent a cornerstone of treatment for advanced gastric cancer (GC). However, their clinical efficacy is hampered by low response rates and the development of both primary and acquired resistance, underscoring the need for innovative combination therapies. In this study, we investigate the potential of Ubenimex, an immunomodulator and inhibitor of leucyl aminopeptidase 3 (LAP3), in enhancing the therapeutic efficacy of PD-L1 blockade in GC. Using a syngeneic GC mouse model, we demonstrate that Ubenimex significantly augments the efficacy of anti-PD-L1 therapy. We further explore the role of LAP3 in GC progression and find that it is highly expressed in both GC tissues and cells, with elevated LAP3 levels correlating with poor prognosis. Functionally, LAP3 facilitates immune evasion through impaired CD8+ T cell infiltration and cytotoxicity in the GC tumor microenvironment (TME). Notably, our findings reveal that LAP3 enhances PD-L1 expression by binding to UBE3A, an E3 ubiquitin ligase. Ubenimex disrupts the LAP3-UBE3A interaction, leading to restored UBE3A-mediated ubiquitination and degradation of PD-L1. This mechanism reinvigorates CD8+ T cell infiltration and cytotoxic activity within the TME, thereby overcoming resistance to anti-PD-L1 therapy. In conclusion, our study provides a strong rationale for the synergistic potential of Ubenimex in combination with PD-1/PD-L1 blockade, offering a promising strategy to overcome current limitations of ICIs therapy in GC patients.

Ovarian cancer is the gynecological malignancy with the highest mortality rate. Platinum resistance remains a major clinical challenge, severely limiting the therapeutic efficacy of cisplatin-based chemotherapy. In recent years, nanomedicine delivery systems have emerged as a promising strategy to enhance the efficacy of conventional cancer treatments. Herein, we constructed a multifunctional graphene oxide-based nanoplatform by functionalizing graphene oxide with hyaluronic acid, gold nanorods, and indocyanine green, followed by loading of cisplatin to form GO-HA-GNRs-ICG@Pt. This nanoplatform exhibits remarkable photothermal and photodynamic conversion efficiency, active tumor-targeting capability, and pH/near-infrared light dual-responsive cisplatin release. More importantly, in vitro and in vivo studies demonstrate that GO-HA-GNRs-ICG@Pt achieves significantly higher therapeutic efficacy and better biosafety compared to cisplatin monotherapy in A2780 ovarian cancer cells. Mechanistically, we discovered that GO-HA-GNRs-ICG@Pt activates the ROS-PINK1/Parkin-mediated mitophagy signaling axis, ultimately enhancing the cisplatin sensitivity of ovarian cancer cells. This work not only provides a theoretical foundation for the development of targeted multifunctional nanoplatforms for integrated cancer therapy but also offers a new synergistic treatment strategy with potential for addressing drug resistance in clinical ovarian cancer.

The clinical utility of docetaxel solution (DTX-sol) is often compromised by limited efficacy and significant side effects. To address these issues, a myristyl alcohol-modified DTX prodrug was designed and synthesized, using a trisulfide bond as a linker arm. High drug loading of DTX prodrug-loaded ferritin nanoparticles (DM FNPs) was achieved using a one-step nano-precipitation method. The resultant DM FNPs exhibited spherical morphology and a uniform size distribution. DM FNPs are activated by tumor-overexpressed glutathione, triggering DTX release, facilitating Fenton reaction-mediated chemodynamic therapy, and inducing self-sensitized ferroptosis. DM FNPs improved the pharmacokinetic behavior of DTX in rats, significantly enhanced the antitumor efficacy, achieving a tumor inhibition rate of 69.57 %, while mitigating adverse reactions to DTX-sol in 4T1 tumor-bearing mice. In conclusion, DM FNPs offer simple and feasible means of enhancing the antitumor efficacy while mitigating adverse effects associated with DTX-sol.

Enzalutamide (ENZ) is clinically used primarily for the treatment of advanced prostate cancer. N-desmethylenzalutamide (NDE) is a primary and biologically active metabolite of ENZ. However, the poor water solubility and oral absorption of ENZ and NDE limit their clinical applications. To develop ENZ and its active metabolites into new formulations, a self-microemulsifying drug delivery system (SMEDDS) for ENZ and NDE was designed to enhance the solubility and antitumor efficacy of these two drugs during delivery. The results indicated that both ENZ-and NDE-SMEDDS exhibited favorable physicochemical properties and in vitro drug release characteristics. In vivo studies revealed that ENZ-and NDE-SMEDDS had higher AUC and half-lives in comparison with that of ENZ-suspensions (ENZ-sus) and NDE-suspensions (NDE-sus). The SMEDDS demonstrates superior antitumor activity compared to ENZ-and NDE-sus, with NDE-SMEDDS showing slightly better antitumor efficacy than ENZ-SMEDDS. The SMEDDS is a potentially novel oral drug delivery system that can enhance the solubility and antitumor effects of ENZ and NDE. Furthermore, as an active metabolite of ENZ, NDE can be developed into new formulations for antitumor application, offering new strategy for the clinical use of NDE.

Traditional cancer therapies, such as chemotherapy, often lack specificity, resulting in severe toxic side effects and limited therapeutic efficacy. There is an urgent need to develop innovative multifunctional nanomedicine carriers that integrate precise diagnosis, targeted therapy, real-time monitoring, and the synergistic effects of multiple therapeutic approaches. In this study, a composite nanodrug delivery system (GO-HA-Ce6-GNRs) based on graphene oxide (GO) was innovatively prepared, which was functionalized with the targeting molecule hyaluronic acid (HA), the photosensitizer chlorin e6 (Ce6), and the photothermal material gold nanorods (GNRs). In vitro and in vivo experiments demonstrated that GO-HA-Ce6-GNRs exhibited excellent biocompatibility, remarkable photothermal and photodynamic properties, high drug-loading capacity for the anticancer drug doxorubicin hydrochloride (DOX), and a dual pH/near-infrared (NIR) light-responsive drug release profile. Additionally, GO-HA-Ce6-GNRs displayed enhanced tumor targeting and efficient fluorescence imaging capabilities. Notably, GO-HA-Ce6-GNRs@DOX manifested highly effective chemotherapy-photothermal-photodynamic synergistic anti-tumor effects in both MCF-7 and HeLa cancer cells as well as U14 tumor-bearing mice. Therefore, GO-HA-Ce6-GNRs@DOX represents a promising nanoplatform for tumor diagnosis and therapy, significantly improving the safety and efficacy of chemotherapy. This work provides a solid foundation and theoretical basis for the development of new targeted nano drug delivery systems that integrate both diagnosis and treatment.

The negative effects of conventional chemotherapy have been significantly reduced in the past several years by the widespread use of nanomedicine delivery systems in conjunction with conventional liver cancer treatments. This study reports the construction of a novel multifunctional nanocomposite by attaching folic acid (FA) and triformylcholic acid (TCA) to the surface of graphene oxide-gold nanospheres (GO-AuNSs). Doxorubicin hydrochloride (DOX) was used as a model drug to form GO-AuNSs-FATCA@DOX on GO-AuNSs-FA-TCA, which has excellent photothermal conversion efficiency, dualtargeted drug delivery, endogenous tumor microenvironment (TME) and near-infrared light (NIR) dual-responsive drug release. More importantly, in vitro and in vivo experiments have shown that the combination therapy shows a higher therapeutic effect than chemotherapy or photothermal therapy alone. Compared with normal cells and other cancer cells, the treatment effect of liver cancer cells is stronger. Therefore, the new nano drug carrier synthesized in this paper has potential application value in the combination therapy of liver cancer. (c) 2025 Published by Elsevier B.V. on behalf of The Society of Powder Technology Japan. All rights are reserved, including those for text and data mining, AI training, and similar technologies.

Background Esophageal cancer (EC), as one of the most common digestive cancers, significantly affects the quality of human life. The aim of this study was to investigate whether matrine-mediated regulation of Cathepsin B (CTSB) affects EC progression. Methods Cell proliferation, apoptosis, and angiogenesis were evaluated using the Methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay, colony formation assay, flow cytometry, and tube formation assay, respectively. Oxidative stress and ferroptosis were assessed by measuring malondialdehyde (MDA), mitochondrial membrane potential (MMP), reactive oxygen species (ROS), and Fe2+ levels using specific commercial assay kits. RT-qPCR and western blotting were utilized to assess mRNA and protein expression, respectively. A mouse xenograft model was established for the purpose of analysis in vivo. Results Matrine significantly suppressed EC cell proliferation and angiogenesis, induced apoptosis, oxidative stress, and ferroptosis, and decreased CTSB expression in EC cells. CTSB was highly expressed in EC tissues and cells. CTSB knockdown inhibited the malignant behavior of EC cells. Conversely, CTSB overexpression reversed the inhibitory effects of matrine on EC cell function. Furthermore, matrine significantly suppressed tumor growth in a xenograft model, accompanied by downregulation of CTSB expression in tumor tissues. Conclusion Matrine suppressed the malignant progression of EC by downregulating CTSB expression, highlighting a potential therapeutic strategy.

Ovarian cancer is a gynecological malignant tumor with the highest mortality rate, and chemotherapy resistance seriously affects patient therapeutic outcomes. It has been shown that the high expression of anti‑apoptotic proteins Bcl‑2 and Bcl‑xL is closely related to ovarian cancer chemotherapy resistance. Therefore, reducing Bcl‑2 and Bcl‑xL expression levels may be essential for reversing drug resistance in ovarian cancer. ABT‑737 is a BH3‑only protein mimetic, which can effectively inhibit the expression of the anti‑apoptotic proteins Bcl‑xL and Bcl‑2. Although it has been shown that ABT‑737 can increase the sensitivity of ovarian cancer cells to cisplatin, the specific molecular mechanism remains unclear and requires further investigation. In the present study, the results revealed that ABT‑737 can significantly increase the activation levels of JNK and ASK1 induced by cisplatin in A2780/DDP cells, which are cisplatin‑resistant ovarian cancer cells. Inhibition of the JNK and ASK1 pathway could significantly reduce cisplatin cytotoxicity increased by ABT‑737 in A2780/DDP cells, while inhibiting the ASK1 pathway could reduce JNK activation. In addition, it was further determined that ABT‑737 could increase reactive oxygen species (ROS) levels in A2780/DDP cells induced by cisplatin. Furthermore, the inhibition of ROS could significantly reduce JNK and ASK1 activation and ABT‑737‑mediated increased cisplatin cytotoxicity in A2780/DDP cells. Overall, the current data identified that activation of the ROS‑ASK1‑JNK signaling axis plays an essential role in the ability of ABT‑737 to increase cisplatin sensitivity in A2780/DDP cells. Therefore, upregulation the ROS‑ASK1‑JNK signaling axis is a potentially novel molecular mechanism by which ABT‑737 can enhance cisplatin sensitivity of ovarian cancer cells. In addition, the present research can also provide new therapeutic strategies and new therapeutic targets for patients with cisplatin‑resistant ovarian cancer with high Bcl‑2/Bcl‑xL expression patterns.

Recently, the advancements in the field of responsive nanomaterials have created new possibilities for restraining the overuse of antibiotics. In this research, we present the fabrication of linear maltodextrin and cyclodextrin polymer (LM-CD) modified graphene oxide (GO) nanocomposites, which were subsequently loaded with levofloxacin (LVN) and oxytetracycline (OXY). The as-prepared nanocomplexes (GO-LM-CD@LVN and GO-LM-CD@OXY) exhibited remarkable synergistic antibacterial efficacy through the combined effects of photothermal therapy and pH-responsive drug delivery, effectively eradicating multidrug-resistant Escherichia coli and Staphylococcus aureus, while concurrently reducing the dosage of antibiotics. The bactericidal rate of 20 mu g mL-1 by GO-LM-CD@LVN and GO-LM-CD@OXY against the aforementioned bacteria was nearly 100% upon NIR irradiation, demonstrating exceptional photothermal properties. In addition, the photochemotherapy effect of GO-LM-CD@LVN was verified by wound healing experiments in mice. The results demonstrated that the application of GO-LM-CD@LVN under NIR irradiation for 10 days resulted in a wound healing rate of approximately 19% higher than that of the blank control group, indicating a remarkable and rapid therapeutic effect. Furthermore, histological analysis using H&E staining revealed no significant impact on the visceral tissues of mice treated with GO-LM-CD@LVN. Collectively, GO-LM-CD is anticipated to serve as a novel photothermal/pH-responsive nanocarrier for achieving efficient antibacterial effects through the synergistic interplay between photothermal materials and antibacterial drugs. GO-LM-CD is anticipated to serve as a novel photothermal/pH-responsive nanocarrier for achieving efficient antibacterial effects through the synergistic interplay between photothermal materials and antibacterial drugs.

The established recognition of N6-methyladenosine (m6A) modification as an indispensable regulatory agent in human cancer is widely accepted. However, the understanding of m6A's role and the mechanisms underlying its contribution to gefitinib resistance is notably limited. Herein, using RT-qPCR, Western blot, Cell proliferation and apoptosis, as well as RNA m6A modification assays, we substantiated that heightened FTO (Fat Mass and Obesity-associated protein) expression substantially underpins the emergence of gefitinib resistance in NSCLC cells. This FTO-driven gefitinib resistance is hinged upon the co-occurrence of PELI3 (Pellino E3 Ubiquitin Protein Ligase Family Member 3) expression and concurrent autophagy activation. Manipulation of PELI3 expression and autophagy activation, including its attenuation, was efficacious in both inducing and overcoming gefitinib resistance within NSCLC cells, as validated in vitro and in vivo. In summary, this study has successfully elucidated the intricate interplay involving FTO-mediated m6A modification, its consequential downstream effect on PELI3, and the concurrent involvement of autophagy in fostering the emergence of gefitinib resistance within the therapeutic context of NSCLC.

Lung cancer is the leading cause of cancer-related deaths worldwide. Combination of drugs targeting independent signaling pathways would effectively block the proliferation of cancer cells with lower concentrations and stronger synergy effects. Dasatinib, a multi-targeted protein tyrosine kinase inhibitor targeting BCR-ABL and kinases of SRC family, has been successfully applied in the treatment of chronic myeloid leukemia (CML). BMS-754807, an inhibitor targeting the insulin-like growth factor 1 receptor (IGF-IR) and insulin receptor (IR) family kinases, has been in phase I development for the treatment of a variety of human cancers. Herein, we demonstrated that dasatinib in combination with BMS-754807 inhibited lung cancer cell growth, while induced autophagy as well as cell cycle arrest at the G1 phase. Dasatinib in combination with BMS-754807 suppressed the expression of cell cycle marker proteins, Rb, p-Rb, CDK4, CDK6 and Cyclin D1, and the PI3K/Akt/mTOR signaling pathway. Dasatinib in combination with BMS-754807 induced autophagy in lung cancer cells, evidenced by the upregulation of LC3B II and beclin-1, the downregulation of LC3B I and SQSTM1/p62, and the autophagic flux observed with a confocal fluorescence microscopy. Furthermore, dasatinib (18 mg/kg) in combination with BMS-754807 (18 mg/kg) inhibited the growth of tumors in NCI-H3255 xenografts without changing the bodyweight. Overall, our results suggest that dasatinib in combination with BMS-754807 inhibits the lung cancer cell proliferation in vitro and tumor growth in vitro, which indicates promising evidence for the application of the drug combination in lung cancer therapy.

The combination of chemo-photothermal therapy with high efficiency and fewer side effects has a good application prospect in cancer treatment. It is of great significance to construct a nano-drug delivery system with cancer cell targeting, high drug loading and excellent photothermal conversion efficiency. Therefore, a novel nano-drug carrier MGO-MDP-FA was successfully constructed by coating folic acid-grafted maltodextrin polymers (MDP-FA) on the surface of Fe3O4-modified graphene oxide (MGO). The nano-drug carrier combined the cancer cell targeting of FA and the magnetic targeting of MGO. A large amount of anti-cancer drug doxorubicin (DOX) was loaded by π-π interaction, hydrogen bond interaction and hydrophobic interaction, with the maximum loading amount and loading capacity of 657.9 mg g-1 and 39.68 wt%, respectively. Based on the excellent photothermal conversion efficiency of MGO, MGO-MDP-FA showed good thermal ablation effect of tumor cells in vitro under NIR irradiation. In addition, MGO-MDP-FA@DOX showed excellent chemo-photothermal synergistic tumor inhibition in vitro (tumor cell killing rate reached 80%). In conclusion, the novel nano-drug delivery system MGO-MDP-FA constructed in this paper provides a promising nano-platform for chemo-photothermal synergistic treatment of cancer.

Background As a three-dimensional network involving glycosaminoglycans (GAGs), proteoglycans (PGs) and other glycoproteins, the role of extracellular matrix (ECM) in tumorigenesis is well revealed. Abnormal glycosylation in liver cancer is correlated with tumorigenesis and chemoresistance. However, the role of galactosyltransferase in HCC (hepatocellular carcinoma) is largely unknown. Methods Here, the oncogenic functions of B4GALT7 (beta-1,4-galactosyltransferase 7) were identified in HCC by a panel of in vitro experiments, including MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), colony formation, transwell and flow cytometry assay. The expression of B4GALT7 in HCC cell lines and tissues were examined by qPCR (real-time quantitative polymerase chain reaction) and western blot assay. The binding between B4GALT7 and miR-338-3p was examined by dual-luciferase reporter assay. Results B4GALT7 encodes galactosyltransferase I and it is highly expressed in HCC cells and human HCC tissues compared with para-tumor specimens. MiR-338-3p was identified to bind the 3′ UTR (untranslated region) of B4GALT7. Highly expressed miR-338-3p suppressed HCC cell invasive abilities and rescued the tumor-promoting effect of B4GALT7 in HCC. ShRNA (short hairpin RNA) mediated B4GALT7 suppression reduced HCC cell invasive abilities, and inhibited the expression of MMP-2 and Erk signaling. Conclusion These findings identified B4GALT7 as a potential prognostic biomarker and therapeutic target for HCC.

GO@LM-SP-FA was constructed by connecting linear maltodextrin polymer and folic acid to the surface of graphene oxide nanoparticles. Doxorubicin hydrochloride was loaded into GO@LM-SP-FA to form GO@LM-SP-FA/DOX, and controlled release of anticancer drugs was realized.

Drug resistance is a critical factor responsible for the recurrence of non-small cell lung cancer (NSCLC). Previous studies suggest that curcumin acts as a chemosensitizer and radiosensitizer in human malignancies, but the underlying mechanism remains elusive. In the present study, we explored how curcumin regulates the expression of miR-142-5p and sensitizes NSCLC cells to crizotinib. We found that miR-142-5p is significantly downregulated in NSCLC tissue samples and cell lines. Curcumin could increase crizotinib cytotoxicity by epigenetically restoring the expression of miR-142-5p. Furthermore, curcumin treatment suppressed the expression of DNA methylation-related enzymes, including DNMT1, DNMT3A, and DNMT3B, in NSCLC cells. In addition, the upregulation of miR-142-5p expression increased crizotinib cytotoxicity and induced apoptosis in tumor cells in a similar manner to that of curcumin. Strikingly, miR-142-5p overexpression suppressed crizotinib-induced autophagy in A549 and H460 cells. Mechanistically, miR-142-5p inhibited autophagy in lung cancer cells by targeting Ulk1. Overexpression of Ulk1 abrogated the miR-142-5p-induced elevation of crizotinib cytotoxicity in A549 and H460 cells. Collectively, our findings demonstrate that curcumin sensitizes NSCLC cells to crizotinib by inactivating autophagy through the regulation of miR-142-5p and its target Ulk1.

Abstract ABT-737, is a BH3-only protein mimetic, which can effectively inhibit the anti-apoptotic proteins Bcl-xL and Bcl-2. A large number of studies have shown that ABT-737 can induce a variety of tumor cell apoptosis, and also enhance cisplatin induced tumor cell apoptosis. However, the mechanism of ABT-737 enhances the sensitivity of ovarian cancer cells to cisplatin is still unclear and needs further study. Our results showed that ABT-737 can significantly increase the sensitivity of A2780/DDP cells to cisplatin. We detected that ABT-737 could significantly increase the activation levels of JNK and ASK1 in A2780/DDP cells induced by cisplatin. Inhibition of JNK and ASK1 pathway could significantly reduce cisplatin sensitivity increased by ABT-737 in A2780/DDP cells, and inhibition of ASK1 pathway could significantly reduce the activation level of JNK. We further detected that ABT-737 could ovbiously increase the level of reactive oxygen species (ROS) in A2780/DDP cells induced by cisplatin, and the inhibition of ROS could significantly reduce the activation levels of JNK and ASK1, as well as could significantly reduce cisplatin sensitivity increased by ABT-737 in A2780/DDP cells. Moreover, calcium chelators can significantly reduce cisplatin sensitivity increased by ABT-737 in A2780/DDP cells, the result is consistent with the current reports. These results suggested that ROS-ASK1-JNK signaling axis and calcium signaling play an important role in ABT-737 reversing cisplatin resistance in ovarian cancer. This might be a novel molecular mechanism of ABT-737 enhances the sensitivity of ovarian cancer cells to cisplatin through regulating ROS-ASK1-JNK signaling axis.

Abstract Introduction: A 73-year-old female patient with right-sided aortic arch and permanent pacemaker installed was brought to Hebei General Hospital because of esophageal perforation at the first esophageal stenosis. Concerns of the patient: She had severe chest pain as well as fever. Despite being treated with fasting, gastrointestinal decompression, anti-inflammation and other methods, but she did not find relief from her pain.Diagnosis: The radiography revealed esophageal perforation at the initial esophageal stenosis. A right-sided aortic arch, anterosuperior mediastinal gas density shadow, and atelectasis of both inferior lobes of the lungs were discovered on a chest CT scan.Intervention: The abscess in the mediastinum was cleaned with surgery, and mediastinal drainage was performed using a thoracoscope. Following the surgery, the patient had underwent ongoing gastric decompression, duodenal feeding, and anti-inflammation therapy.Outcomes: The patient was successfully fed and discharged from the hospital on the 14 postoperative day.Conclusion: The therapeutic management of this condition was hampered by a number of reasons. The most important thing is to identify the major inconsistency, select a good surgical approach, and develop an adequate perioperative care strategy.