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Abstract Background This retrospective study aimed to assess the safety and efficacy of microwave ablation for lung tumors adjacent to the interlobar fissures. Methods From May 2020 to April 2021, 59 patients with 66 lung tumors (mean diameter, 16.9 ± 7.7 mm; range, 6–30 mm) adjacent to the interlobar fissures who underwent microwave ablation at our institution were identified and included in this study. Based on the relationship between the tumor and the interlobar fissure, tumors can be categorized into close to the fissure, causing the fissure, and involving the fissure. The complete ablation rate, local progression‐free survival, complications, and associated factors were analyzed. Results All 66 histologically proven tumors were treated using computed tomography‐guided microwave ablation. The complete ablation rate was 95.5%. Local progression‐free survival at 3, 6, 9, and 12 months were 89.4%, 83.3%, 74.2%, and 63.6%, respectively. The complications included pneumothorax (34.8%), pleural effusion (24.2%), cavity (18.2%), and pulmonary infection (7.6%). There were statistical differences in the incidence of pneumothorax, cavity, and delayed complications between the groups with and without antenna punctures through the fissure. Conclusions Microwave ablation is a safe and effective treatment for lung tumor adjacent to the interlobar fissure. Antenna puncturing though the interlobar fissure may be a potential risk factor for pneumothorax, cavity, and delayed complications.

Background Scutellarin (SCU), a flavonoid isolated from Erigeron breviscapus (Vant.) Hand.‐Mazz., increases autophagy and apoptosis in the adenocarcinoma A549 cell line, which is resistant to cisplatin. However, whether SCU alone has antitumor activity against non‐small cell lung cancer (NSCLC) is unknown. Methods Cell Counting Kit‐8, flow cytometry, colony formation, Hoechst 33258 staining, and Western blot analyses were used to examine the proliferation and apoptosis of A549 cells treated with SCU and the possible molecular mechanisms. Results The cell viability assay indicated that SCU markedly suppressed the proliferation of A549 cells in concentration and time‐dependent manners. SCU caused significant G0/G1 phase arrest and apoptosis, as evidenced by flow cytometric analyses, Hoechst 33258 staining, and Western blot analyses of cyclin D1, cyclin E, BCL‐2, cleaved‐caspase‐3, and BAX. Furthermore, SCU treatment reduced the level of pan‐AKT, phosphorylated (p)‐mTOR, mTOR, BCL‐XL, STAT3, and p‐STAT3, and increased the level of 4EBP1. Conclusions SCU can suppress proliferation and promote apoptosis in A549 cells through AKT/mTOR/4EBP1 and STAT3 pathways. This suggests that SCU may be developed into a promising antitumor agent for treating NSCLC.