Background: Circular RNAs (circRNAs) are regarded as vital regulatory factors in various cancers. However, the biological functions of circDNER in the paclitaxel (PTX) resistance of lung cancer remain largely unexplored.Methods: Quantitative reverse transcription polymerase chain reaction (qRT‐PCR) was used to analyze circDNER, miR‐139‐5p, and ITGB8. Cell proliferation was assessed via colony formation and MTT assays. Cell apoptosis was evaluated by flow cytometry. Western blot was performed to assess protein expression. The targeted interaction among circDNER, miR‐139‐5p, and ITGB8 were validated using dual‐luciferase reporter or RNA immunoprecipitation assays.Results: Inhibition of circDNER reduced IC50 of PTX, inhibited cell proliferation, invasion and migration, as well as promoted cell apoptosis in PTX‐resistant lung cancer cells. Mechanistically, circDNER sponged miR‐139‐5p to upregulate ITGB8 expression. Overexpression of miR‐139‐5p reversed the biological functions mediated by circDNER in PTX‐resistant lung cancer cells. MiR‐139‐5p overexpression suppressed PTX resistance and malignant behaviors of PTX‐resistant lung cancer cells, with ITGB8 elevation rescued the impacts. Moreover, we demonstrated that circDNER was upregulated in plasma exosomes from lung cancer patients. The plasma exosomes derived from these patients are the key factors enhancing the migration and invasion potential of lung cancer cells.Conclusion: The circDNER mediated miR‐139‐5p/ITGB8 axis suppresses lung cancer progression. Our findings suggest that circDNER might act as a potential prognostic biomarker and therapeutic target for lung cancer treatment.

The use of immune checkpoint inhibitors that target programmed cell death‐1 (PD‐1) has been proposed for the treatment of advanced non‐small cell lung cancer (NSCLC). However, in clinical trials, cumulative response rates to anti‐PD‐1 treatment were approximately 20% in patients with NSCLC. CCR4‐NOT transcription complex, subunit 4 (CNOT4) is a RING finger protein with E3 ubiquitin ligase activity. We previously reported that CNOT4 may act as a tumor suppressor in NSCLC. Here, we examined whether CNOT4 can enhance the efficacy of anti‐PD‐1 immunotherapy in a model of NSCLC. The association of CNOT4 and overall survival was analyzed using datasets from The Cancer Genome Atlas (TCGA). Tumor models were established by subcutaneously implanting tumor cells line (A549 cell) into mice. CNOT4 was observed to be positively associated with relapse‐free survival and overall survival in patients with NSCLC. CNOT4 overexpression suppressed tumor growth in vivo and enhanced the effect of anti‐PD‐1 immunotherapy, which was accompanied by increased CD3⁺ and CD8⁺ T lymphocyte infiltration and higher interferon‐γ and tumor necrosis factor‐α levels. In conclusion, CNOT4 may enhance the efficacy of anti‐PD‐1 immunotherapy and may have potential as a prognostic marker for NSCLC, or as a combinational target with anti‐PD‐1 treatment for patients with NSCLC.

Esophageal squamous cell carcinoma (ESCC) remains a lethal malignancy with limited therapeutic options. This study investigated the antitumor efficacy and mechanisms of decursin, a natural pyranocoumarin derivative, against ESCC. In vitro analyses demonstrated that decursin selectively inhibited ESCC cell viability (IC50: 14.62 ± 0.61–26.20 ± 2.11 μM across TE-1, KYSE-30, and KYSE-150 cell lines) without affecting normal esophageal epithelial cells (Het-1A). Decursin (10 μM) suppressed colony formation, impaired wound healing (p < 0.001 at 48 h), and reduced Transwell migration/invasion in KYSE-150 cells. Subcutaneous xenograft models revealed significant tumor growth inhibition (p < 0.01) with decursin treatment (10 mg/kg, intraperitoneal), accompanied by no systemic toxicity. Mechanistically, decursin induced G0/G1 cell cycle deceleration (p < 0.01) and apoptosis through ubiquitin–proteasome-mediated degradation of oncoproteins TP63 and SOX2. Time- and dose-dependent protein suppression was reversed by proteasome inhibitor MG-132, but unaffected by lysosomal inhibition. These findings establish decursin as a promising therapeutic agent for ESCC, functioning via proteasomal degradation of key oncogenic drivers, and provide a rationale for decursin’s further development as a targeted monotherapy or chemosensitizer in multimodal regimens.

The purpose of this study was to evaluate the changes in pulmonary function after wedge resection, segmentectomy, and lobectomy. The patients were divided into 4 groups: lobectomy group, segmentectomy group, wedge resection group, and mediastinal surgery group. The pulmonary function was evaluated at various time points: 3 days before surgery, 1 month, 6 months, 12 months, and then 24 months after surgery. The analysis results of forced expiratory volume in one second difference and breath-holding tests difference were consistent: Lobectomy group was higher than segmentectomy group, wedge resection group, and mediastinal surgery group at 4 postoperative time points (P < .05); segmentectomy group was higher than the wedge resection group and mediastinal surgery group (P < .05), and there was no statistical difference between the wedge resection group and the mediastinal surgery group (P > .05). Analysis results of tidal volume difference: Lobectomy group was higher than segmentectomy group, wedge resection group, and mediastinal surgery group at 4 postoperative time points (P < .05); segmentectomy group was higher than wedge resection group and mediastinal surgery group at 1 month after surgery (P < .05). Analysis results of the diffusion capacity of the lung for carbon monoxide difference: lobectomy group and segmentectomy group were higher than wedge resection group and mediastinal surgery group at 4 postoperative time points (P < .05). Analysis results of the stair-climbing test difference: lobectomy group and segmentectomy group were higher than the wedge resection group and mediastinal surgery group at 4 postoperative time points (P < .05). Segmentectomy was superior to lobectomy in the protection of pulmonary function, while wedge resection was superior to segmentectomy. The recovery process of the pulmonary function was the fastest during the first 6 months after surgery.