Lung adenocarcinoma (LUAD) metastasis is a major cause of patient mortality, with the key mechanism being the resistance of tumor cells to anoikis. HILPDA is associated with tumor progression, but its role and mechanism in anoikis in LUAD remain unclear. Bioinformatics analysis and single-cell sequencing dataset analysis were performed to investigate HILPDA expression in LUAD and its prognostic value, with its expression in cells validated. An anoikis-resistant A549 cell line variant (A549-AR) was established, and the effects of HILPDA on its resistance, migration, and invasion were assessed using CCK-8, trypan blue staining, flow cytometry, wound healing assay, and transwell. Western blot (WB) confirmed protein expression changes. Immunofluorescence microscopy revealed HILPDA's colocalization with lipid droplets, and Oil Red O staining and biochemical assays quantified lipid accumulation. Bioinformatics screening identified FOXA1 as a potential upstream regulator of HILPDA. ChIP-qPCR and dual-luciferase reporter assays validated the regulatory role of FOXA1 over HILPDA. A xenograft mouse model was used to evaluate tumor size and lipid accumulation. In LUAD, HILPDA expression was distinctly elevated, correlating with a worse prognosis. Silencing HILPDA markedly curtailed the viability, proliferation, migration, and invasion of A549-AR cells, and weakened their anti-apoptotic capacity. HILPDA overexpression bolstered malignancy by augmenting lipid droplet accumulation. FOXA1 transcriptionally activated HILPDA, which increased lipid droplet accumulation and promoted anoikis resistance and metastatic potential in A549-AR cells. FOXA1 promotes lipid droplet accumulation by transcriptionally activating HILPDA, leading to LUAD anoikis resistance and metastasis. HILPDA may serve as a potential therapeutic target for LUAD metastasis.

e16115 Background: Neoadjuvant chemoradiotherapy (nCRT) or neoadjuvant chemotherapy (nCT) followed by esophagectomy has been taken as the currently the standard of care for patients with locally advanced esophageal squamous cell carcinoma (LA-ESCC). However, both model were still limited by the relative high incidence of recurrence and poor prognosis. This phase II study aims to explore the efficacy and safety of a new neoadjuvant treatment combination of Envafolimab, Albumin-bound Paclitaxel and Cisplatin for LA-ESCC. Methods: This is a prospective, single-arm multicenter Phase II study. Eligible patients with pathologically confirmed ESCC and at clinical T1-3N1-3M0 or T3N0M0 stage according to the eighth edition of American Joint Committee on Cancer (AJCC) are included. The regimen includes 2 cycles of envafolimab subcutaneously at 300mg(d1), albumin-bound Paclitaxel Intravenously at 100mg/㎡ (d1 and d8), and cisplatin Intravenously at 75 mg/㎡(d1).The primary endpoint is pathological complete response (pCR) rate. Results: As of December 11, 2024, a total of 32 patients were included from four institutions in this study. Among them, 29 were male, and three were female. The median age of the patients was 64.5 years. Most patients(31/32,96.88%) finished two cycles neoadjuvant treatment. One patient occurred cerebral hemorrhage,and the other three patients chosed close observation rather than esophagectomy after two cycles neoadjuvant treatment. Total 28 patients underwent surgery, of which 9 patients achieved PCR (9/28,32.14%), 23 patients achieved at least major pathological response(MPR) (23 / 28, 82.14%), and other 5 patients did not achieve MPR. Conclusions: The combination of envafolimab, albumin-bound paclitaxel and cisplatindemonstrates promising pCR rate and acceptable tolerance in patients with LA-ESCC. The trial is ongoing, with further investigation anticipated. Clinical trial information: NCT05828381 .

TNF receptor-associated factor 3 interacting protein 3 (TRAF3IP3/T3JAM) exhibits dual roles in cancer progression. While upregulated in most malignancies and critical for immune regulation. However, the specific effects and molecular mechanisms of TRAF3IP3 on the progression of lung adenocarcinoma (LUAD) remains poorly understood. This study reveals TRAF3IP3 is upregulated in several tumor tissues but exclusively decreased in LUAD and Lung squamous cell carcinoma (LUSC) tissues, consequential in a favorable overall survival (OS) in LUAD rather than LUSC. Herein, it is reported that TRAF3IP3 can suppress cell proliferation and promote the apoptosis rate of LUAD cells by inducing excessive ER stress-related apoptosis. Importantly, TRAF3IP3 triggers ER stress via the PERK/ATF4/CHOP pathway, accompanied by stimulated ER stress-induced cytoprotective autophagy in LUAD cells. Through IP-MS analysis, STRN3 is identified as a direct downstream interactor with TRAF3IP3 and corroborated to regulate ER stress positively. Mechanistically, TRAF3IP3 facilitates the recruitment of STRN3 to the ER lumen through its transmembrane domain and fulfills its functional role in ER stress in an STRN3-dependent manner in LUAD cells. Given its dual role in orchestrating ER stress-associated apoptosis and autophagy in LUAD cell fate determination, the importance of TRAF3IP3 is highlighted as novel therapeutic target for LUAD treatment.

Background:The rate of postoperative complications in wedge resection is low because it does not involve major structures. However, postoperative air leakage (AL) is common. This research sought to determine the risk factors associated with AL following thoracoscopic pulmonary wedge resection and to create a predictive model for identifying patients suitable for tubeless procedures. Methods:This study included individuals who underwent thoracoscopic pulmonary wedge resection at Fujian Medical University Union Hospital from January 2015 to December 2020. Univariate and multivariate logistic regression analyses were conducted to identify independent risk factors and construct relevant models. Concurrent data from two other centers were collected as validation sets for external validation. Results:A total of 2,503 patients meeting the inclusion criteria were included in the study, with an overall incidence of AL at 11.35% (284/2,503). The development dataset included 2,006 cases, and columnar plots were drawn based on the outcomes of the multivariate logistic regression analysis. The final model included age >70, forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) ratio (FEV1%) <80%, nodule size, benignity/malignancy, and pleural adhesions (none, focal, diffuse). In the development dataset, the C-index was 0.829. The external validation set included 497 cases, with a C-index of 0.833. Conclusions:The AL prediction model performed well and may be clinically useful for assessing AL and identifying patients who can benefit from tubeless strategies.

Interstitial lung abnormality (ILA) has been recognized as a pertinent factor in the development and prognosis of various pulmonary conditions. However, its correlation with co-morbidities remains understudied. The current study endeavors to elucidate the association between ILA and both clinical features and co-morbidities in patients with chronic obstructive pulmonary disease (COPD). A retrospective cohort comprising 1131 hospitalized patients diagnosed with COPD was examined in this observational study. Patients were dichotomously classified based on the presence or absence of ILA, and subsequent analyses scrutinized disparities in demographic, clinical, and laboratory profiles, alongside co-morbid conditions, between the two subgroups. Of the 1131 COPD patients, 165 (14.6

AbstractObjectiveNon‐small cell lung cancer (NSCLC) occupies 85% of lung cancer. Long non‐coding RNAs (LncRNAs) can regulate the radiosensitivity of cancers. This study explored the mechanism of lncRNA TRERNA1 in the radiosensitivity of NSCLC cells.MethodsLncRNA TRERNA1 level in NSCLC cell lines was determined. NSCLC cell radiation tolerance was measured. TRERNA1 expression was silenced or overexpressed in A549/HCC827 cells with the highest/lowest radiation tolerance, respectively. The contents of γ‐H2AX and SA‐β‐gal in NSCLC cells after radiation induction were detected. The targeted binding of TRERNA1 to miR‐22‐3p and miR‐22‐3p to SP1 were verified by dual‐luciferase assay. SP1 expression were detected. Functional rescue experiments were implemented to confirm the roles of miR‐22‐3p and SP1 in the regulatory mechanism of TRERNA1.ResultsTRERNA1 was upregulated in NSCLC cells. TRERNA1 silencing enhanced radiosensitivity of NSCLC cells. TRERNA1 silencing elevated the contents of γ‐H2AX and SA‐β‐gal in A549 cells after radiation induction, while TRERNA1 overexpression showed an opposite trend in HCC827 cells. There were targeting relationships between TRERNA1 and miR‐22‐3p, and miR‐22‐3p and SP1. miR‐22‐3p repression or SP1 overexpression abolished the effects of TRERNA1 silencing.ConclusionTRERNA1 silencing enhanced radiosensitivity of NSCLC cells via the miR‐22‐3p/SP1 axis. This study may offer new targets for NSCLC treatment.

Introduction:Preoperative computed tomography (CT)-guided localization can shorten the time of video-assisted thoracoscopic surgery (VATS) and accurately aid in pulmonary nodule removal.Aim:To discuss the application value and safety of 2 kinds of breast localization needles and anchor localization needles in clinical practice for pulmonary nodules under CT guidance before VATS.Material and methods:We retrospectively studied 215 patients with 247 pulmonary nodules, who underwent CT-guided pulmonary nodule location before VATS. The 2 kinds of localization needles were randomly used, and we collected and analysed the clinical data.Results:We used breast and anchor localization needles in 27.9% and 72.1% of cases, respectively. Differences were observed in puncture localization time, detachment rate, and visual analogue scale (VAS). The detachment rate (0%) and positioning time (median: 12 min) were less in the anchor than in the breast localization needle group (8.7% and median: 13 min, respectively). The median VAS was approximately 2 and 5 in the anchor and breast localization needle groups, respectively. Surgical pathology revealed that 155 (62.8%) pulmonary nodules were malignant while 92 (37.2%) were benign. The primary distinction in surgical procedures is the higher proportion of segmental resections in the middle and inner band group (19.3%) compared to the periphery band group (4.2%).Conclusions:Unlike breast localization needles, anchor localization needles can reduce pain and discomfort after positioning, and they are not easy to decouple. These 2 needles are safe for CT-guided localization, which can shorten the time of VATS and accurately aid in pulmonary nodule removal.

BACKGROUND:Low quality of life (QoL) in patients with non-small cell lung cancer (NSCLC) receiving adjuvant chemotherapy after radical resection is a major global health issue. High-quality evidence for the effectiveness of Shenlingcao oral liquid (SOL) as a complementary treatment in this patients is lacking at present. PURPOSE:To determine whether complementary SOL treatment in NSCLC patients receiving adjuvant chemotherapy would yield greater improvements in QoL than chemotherapy alone. STUDY DESIGN:We conducted a multicenter, randomized controlled trial of stages IIA-IIIA NSCLC patients undergoing adjuvant chemotherapy in seven hospitals. METHODS:Using stratified blocks, participants were randomized in a 1:1 ratio to receive SOL combined with conventional chemotherapy or conventional chemotherapy alone. The primary outcome was the change in global QoL from baseline to the fourth chemotherapy cycle, and intention-to-treat analysis was applied with a mixed-effect model. Secondary outcomes were functional QoL, symptoms, and performance status scores at the 6-month follow-up. Missing data were handled with multiple imputation and a pattern-mixture model. RESULTS:Among 516 randomized patients, 446 (86.43%) completed the study. After the fourth chemotherapy cycle, in comparison with the control group, patients receiving SOL showed a lower reduction in mean global QoL (-2.76 vs. -14.11; mean difference [MD], 11.34; 95% confidence interval [CI], 8.28 to 14.41), greater improvement in physical function (MD, 11.61; 95% CI, 8.57 to 14.65), role function (MD, 10.15; 95% CI, 5.75 to 14.54), and emotional function (MD, 4.71; 95% CI, 1.85 to 7.57), and greater improvements in lung cancer-related symptoms (e.g., fatigue, nausea/vomiting, and appetite loss) and performance status during the 6-month follow-up period (treatment main effect, p < 0.05). CONCLUSION:SOL treatment for NSCLC patients receiving adjuvant chemotherapy can significantly improve QoL and performance status within 6 months after radical resection. TRIAL REGISTRATION:ClinicalTrials.gov identifier: NCT03712969.

Objective To explore the effect of ophiopogonin B(OP-B) on the biological behavior of esophageal squamous cell carcinoma cell line(EC9706) and its mechanism related to the regulation of Down syndrome cell adhesion molecule antisense 1 (DSCAM-AS1) and miR-199a-3p expression. Methods EC9706 cells were divided into control group, experiment groups with low, medium and high dosage of OP-B, si-NC group, si-DSCAM-AS1 group and (pcDNA-DSCAM-AS1+OP-B) group. Colony formation and CCK-8 method were used to detect EC9706 proliferation. Flow cytometry and scratch healing test were used to analyze the apoptosis rate and migration of EC9706 cells. RT-qPCR was performed to detect the expression of DSCAM-AS1 and miR-199a-3p. The targeting relationship between DSCAM-AS1 and miR-199a-3p was verified using dual luciferase reporter gene experiment. Results OP-B reduced EC9706 viability, colony formation counting, migration distance and DSCAM-AS1 expression (P＜0.05), increased cell apoptosis rate and miR-199a-3p expression (P＜0.05). DSCAM-AS1 interacted directly with miR-199a-3p. After interference to DSCAM-AS1 expression, the cell viability, colony formation and migration distance of EC9706 cells were significantly reduced(P＜0.05), while apoptosis rates were significantly increased(P＜0.05). Over-expression of DSCAM-AS1 antagonized the effects of OP-B on the proliferation, apoptosis and migration of EC9706 cells(P＜0.05). Conclusions OP-B inhibits proliferation and migration of esophageal squamous cell carcinoma cells and induces cell apoptosis. The mechanism is potentially explained by down-regulating DSCAM-AS1/miR-199a-3p pathway.

Abstract Background Lung cancers arising in never smokers have been suggested to be substantially different from lung cancers in smokers at an epidemiological, genetic and molecular level. Focusing on non-small cell lung cancer (NSCLC), we characterized lung cancer patients in China looking for demographic and clinical differences between the smoking and never-smoking subgroups. Methods In total, 891 patients with NSCLC, including 841 with adenocarcinoma and 50 with squamous cell carcinoma, were recruited in this study. Association of smoking status with demographic and clinical features of NSCLC was determined, and risk factors for lymph node metastasis and TNM stage were evaluated using Multivariate logistic regression analysis. Results In patients with adenocarcinoma, never smokers showed a younger age at diagnosis (54.2 ± 12.7vs. 59.3 ± 9.4, p adjusted <0.001), a lower risk for lymph node metastasis than smokers (7,6% vs. 19.5%, p adjusted <0.001) and less severe disease as indicated by lower percentages of patients with TNM stage of III or IV (5.5% vs. 14.7%, p adjusted <0.001 ). By contrast, these associations were not observed in 50 patients with squamous cell carcinoma. Multivariate logistic regression analysis showed that smoking status was a risk factor for lymph node metastasis (OR = 2.70, 95% CI: 1.39–5.31, p = 0.004) but not for TNM stage (OR = 1.18, 95% CI: 0.09–14.43, p = 0.896) in adenocarcinoma. Conclusion This study demonstrates that lung adenocarcinoma in never smokers significantly differ from those in smokers regarding both age at diagnosis and risk of lymph node metastasis, supporting the notion that they are distinct entries with different etiology and pathogenesis.

目的 分析肺结节结构化电子病历是否有助于住院医师规范化培训学员(住培学员)掌握肺结节患者的门诊和住院管理能力.方法 本研究纳入2018年1月-2021年1月在厦门大学附属第一医院外科住院医生规范化培训基地接受培训的120名学员,其中男94人、女26人,年龄22～31(26.45±2.81)岁.随机分为两组,分别使用我科设计的肺结节结构化电子病历(结构化组)和外科通用非结构化电子病历(非结构化组),分析比较两组学员在住院病历撰写时间、首次病程记录完成时间、病程记录的病历质量、开具入院医嘱的准确率、进行教学查房的质量、患者满意度等方面的差异.结果 (1)结构化组住培学员住院病历撰写时间显著短于非结构化组[(53.61±8.12)min vs.(84.25±16.09)min,P＜0.010];同样,结构化组首次病程记录完成时间短于非结构化组,且差异有统计学意义[(13.20±5.43)min vs.(27.51±8.62)min,P＜0.010].(2)结构化组学员教学查房质量评分总体显著高于非结构化组,且差异有统计学意义[(84.21±15.61)分vs.(70.91±12.28)分,P＜0.010].(3)结构化组学员病历书写质量评分显著高于非结构化组,且差异有统计学意义[(80.25±9.22)分vs.(74.22±5.40)分,P＜0.010].结论 肺结节结构化电子病历在外科住院医师规范化培训中能有效提高培训效果,提高学员处理肺结节的临床业务能力,提高学员采集关键临床数据的完整性和准确性,改善医患关系.

目的： 探讨下咽、食管多原发癌（multiple primary carcinoma，MPC）的治疗及预后。 方法： 回顾性分析2013—2018年厦门大学附属第一医院收住院进行手术的67例下咽、食管同时性MPC患者的病例资料，其中男65例，女2例，年龄42~79岁。分析患者的一般资料、手术决策、术后并发症及随访情况。采用SPSS 22.0 软件行Kaplan Meier法计算生存率，使用Logrank检验和单因素预后分析，Cox模型进行多因素预后分析。 结果： 67例患者行一期胸腔镜辅助下全喉、下咽、食管切除并管状胃重建手术38例；一期内镜下食管黏膜剥离术，二期行下咽癌扩大切除术24例；一期内镜下食管黏膜剥离并下咽癌经口激光切除术2例；一期下咽癌经口激光切除术，二期胸外科食管癌根治术3例。术后并发症包括肺部感染18例次、胸腔积液3例次、气管撕裂1例次、乳糜漏1例次、腹水1例次；无吻合口瘘及围手术期死亡病例。术前诱导化疗8例，术后转放疗科同步放化疗51例。1年总生存率82.1%，3年总生存率 55.9%。在下咽、食管同时性MPC中下咽癌分期、食管癌分期、肿瘤家族史以及重度吸烟饮酒史与预后相关（χ²值为6.602、7.422、5.932、6.236，P值均<0.05）。 结论： 对于下咽食管MPC的治疗除微创手术外，尽量避免分期根治性手术，手术切除结合放化疗的综合治疗理念是目前下咽癌同时性食管癌较为理想的治疗方案。.

Abstract Background A pathologically confirmed negative margin is required when performing sublobar resection in patients with early stage peripheral lung adenocarcinoma. However, the optimal margin distance to ensure complete tumor resection while preserving healthy lung tissue remains unknown. We aimed to establish a reliable distance range for negative margins. Methods A total of 52 intraoperative para-cancer tissue specimens from patients with peripheral lung adenocarcinoma with pathological tumors ≤2 cm in size were examined. Depending on the distance from the tumor edge (D), the para-cancer tissues were divided into the following five groups: D < 0.5 cm (group I); 0.5 cm ≤ D < 1.0 cm (group II); 1.0 cm ≤ D < 1.5 cm (group III); 1.5 cm ≤ D < 2.0 cm (group IV); and D ≥ 2.0 cm (group V). During pathological examination of the specimens under a microscope, the presence of atypical adenomatous hyperplasia or more severe lesions was considered unsafe, whereas the presence of normal lung tissue or benign hyperplasia was considered safe. Results Group V, in which the margin was the farthest from the tumor edge, was the safest. There were significant safety differences in between groups I and V (χ2 = 26.217, P < 0.001). Significant safety differences also existed between groups II and V (χ2 = 9.420, P < 0.005). There were no significant safety differences between group III or IV and group V (P = 0.207; P = 0.610). Conclusions We suggest that when performing sublobar resection in patients with early stage peripheral lung adenocarcinoma with pathological tumor sizes ≤2 cm, the resection margin distance should be ≥1 cm to ensure a negative margin.

BACKGROUND:Long intergenic non-protein coding RNA 1140 (LINC01140), a long non-coding RNA, is highly expressed in various cancers; however, its biological functions in lung cancer (LC) progression and immune escape are still unclear. METHODS:Here, to elucidate LINC01140 function, 79 paired LC and paracancerous tissues were collected. LINC01140 expression levels were determined using fluorescence in situ hybridization and qPCR analysis. Cell counting kit-8 (CCK-8) assay and transwell assays were performed. The interaction between microRNAs (miRNAs) and LINC01140 was confirmed using an RNA immunoprecipitation assay. Cytokine-induced killer (CIK) cell phenotypes were analyzed by flow cytometry. Cytokine secretion levels were determined by ELISA. CIK cytotoxicity was assessed by measuring lactate dehydrogenase release. Besides, xenograft tumor mouse models were used to unveil the in vivo function of LINC01140. RESULTS:We found that LINC01140 was highly expressed in human LC tissues and cell lines. High LINC01140 levels were associated with poor survival in patients with LC. LINC01140 upregulation promoted the proliferation, migration, and invasion of LC cells through direct interaction with miR-33a-5p and miR-33b-5p, thereby contributing to c-Myc expression and also inhibited cisplatin-induced cell apoptosis. In subcutaneous tumor xenograft mice, LINC01140 knockdown markedly reduced tumor growth and lung metastasis. Additionally, LINC01140 directly repressed miR-377-3 p and miR-155-5 p expression levels, resulting in the upregulation of their common downstream target programmed death-ligand 1 (PD-L1), a crucial target in LC immunotherapy. Notably, we proved that LINC01140 knockdown, along with CIK administration, suppressed the growth of subcutaneous LC xenografts by decreasing PD-L1 expression in severe combined immunodeficient mice. CONCLUSIONS:Taken together, LINC01140 overexpression protects c-Myc and PD-L1 mRNA from miRNA-mediated inhibition and contributes to the proliferation, migration, invasion, and immune escape of LC cells. These results provide a theoretical basis that LINC01140 is a promising target for LC treatment.

ABSTRACT A 50-year-old woman with a newly detected pulmonary ground-glass opacity (GGO) nodule underwent PET/CT to determine the likelihood of malignancy. This patient was enrolled in the prospective study (NCT04588064) to determine the effectiveness of 18F-FDG and 68Ga-FAPI PET/CT for characterization of the GGO nodule. On PET/CT images, minimal 18F-FDG uptake but intense 68Ga-FAPI uptake was observed in this GGO nodule. This patient subsequently underwent video-assisted thoracoscopic surgery, and postoperative pathological examination confirmed the diagnosis of invasive adenocarcinoma. This case presented an example where 68Ga-FAPI PET/CT showed higher tracer uptake than 18F-FDG in the malignant GGO nodule.

1Department of Medical Oncology, Xiamen Key Laboratory of Antitumor Drug Transformation Research, Cancer Center, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian Province 361003, People’s Republic of China; 2Teaching Hospital of Fujian Medical University, Xiamen, Fujian Province 361003, People’s Republic of China; 3Department of Thoracic Surgery, The First Affiliated Hospital of Xiamen University, Teaching Hospital of Fujian Medical University, Xiamen, Fujian Province 361003, People’s Republic of China

目的 通过肺结节交互印证式诊断,提高术前影像诊断的准确率,选择合适的手术时机,指导肺小结节的随访时间.方法 回顾性分析单中心2016年7月至2019年10月厦门大学附属第一医院胸外科1 368例肺结节手术患者的临床资料,男531例、女837例,年龄44(21～67)岁.选择肺结节直径≤2 cm,术前行多学科会诊,详细阅读胸部CT,术中切开病灶剖面进行分析,快速病理诊断肺结节性质,术后常规行病理诊断.随后将肺结节影像特征、术中剖面特征与病理结果一一对照,通过两两对应,交互印证,把肺结节的影像病理及病变切面表现为一个动态变化的过程.结果 在1 368例肺小结节患者中,影像学表现为纯磨玻璃样结节的有376例(27.5％),混合性磨玻璃样结节共有729例(53.3％),实性结节共有263例(19.2％).在纯磨玻璃样结节患者中,原位腺癌(adenocarcinoma in situ,AIS)占比最高,为156例,微浸润性腺癌(microinvasive adenocarcinoma,MIA)和不典型腺瘤样增生(atypical adenomatous hyperplasia,AAH)比例相当,分别为90例和85例,其它良性肿瘤共20例.在混合性磨玻璃样结节中,浸润性腺癌(invasive adenocarcinoma,IA)共495例,其次是MIA 207例;且在实性结节中,病理结果主要为IA和其它良性肿瘤,分别为213例和50例,实性结节病理无AAH、AIS及MIA.结论 肺结节交互印证式诊断可以提高术前诊断的准确率,对选择手术时机、随访时间的判断具有重要意义.

Introduction Lung adenocarcinoma (LUAD), which is associated with high morbidity and mortality, is prone to cisplatin resistance, resulting in poor patient prognosis. Long non-coding RNAs (lncRNAs) have complex biological functions in a variety of tumors. Elucidating the underlying molecular mechanisms between lncRNA and cisplatin resistance in LUAD is expected to enable identification of new targets for drug development. Methods Cell proliferation was measured by CCK-8 assay and cell apoptosis was detected using flow cytometry analysis. Luciferase reporter assay was conducted to determine the interaction between lncRNA and MicroRNA. Gene expression was evaluated by Real-Time Quantitative Reverse Transcription Polymerase Chain Reaction and Western blot analysis. Results Long non-coding RNA activated by TGF-β (lncRNA-ATB) was shown to be significantly up-regulated in A549 cells resistant to cisplatin/cis-dichlorodiammineplatinum (II) (cis-DDP) (A549/CDDP cells), compared with corresponding levels in parental A549 cells. Overexpression of lncRNA-ATB significantly elevated cisplatin resistance in LUAD cell lines (A549 and H1975 cells), and this was associated with activation of apoptosis-related genes. Conversely, silencing of lncRNA-ATB decreased cisplatin resistance in LUAD cells. Mechanistically, lncRNA-ATB increased expression of β-catenin by directly binding to MicroRNA-200a (miR-200a), thereby promoting cell survival and cisplatin resistance. Transfection with a miR-200a mimic or treatment with the β-catenin downstream pathway inhibitor IWR-1 could reverse the phenotypes induced by lncRNA-ATB overexpression. Conclusion In summary, this study revealed that lncRNA-ATB is dramatically up-regulated in cisplatin-resistant LUAD cell lines, and that lncRNA-ATB facilitates cell survival by targeting the miR-200a/β-catenin pathway in these cells.

Objective:To investigate the difference of HRCT imaging features between COVID-19 and the ground-glass opacity(GGO) lesion of early-stage lung carcinoma, standardize the diagnosis and treatment process of ground-glass opacity(GGO) degeneration during the epidemic.Methods:A total of 34 patients with diagnosed COVID-19 who confirmed by positive results of the new coronavirus nucleic acid test were collected as observation group 40 patients with pathologically diagnosed early-stage lung carcinoma whose preoperative HRCT examination showed pure ground glass lesions and received surgical intervention were recruited from the Department of Thoracic Surgery (The First Affiliated Hospital of Xiamen University) from January 2018 to December 2019 as the control group. The HRCT imaging features of these two groups of patients were compared and statistically analyzed.Results:The HRCT imaging features of the new type of COVID-19 showed significant difference by characteristics of multiple lesions, lesion rapid variation within 3 days, reticular pattern, vacuolar sign and clear boundary compared to the GGO lesion of early-stage lung carcinoma( P<0.05). The chinical and imaging characteristic the sex, age, with pleural effusion or not and the lesion location showed no significant difference between these 2 groups ( P>0.05). Conclusion:Contrast with inert early lung carcinoma lesions, COVID-19 disease developed rapidly. Imaging dynamic examination can provide evidences to distinguish Novel Coronavirus Pneumonia and early-stage lung carcinoma.

Paraneoplastic autoimmune disorders (PAD) represent a group of autoimmune diseases associated with neoplasms. As a consequence of a remote autoimmunity-mediated effect, PAD are found in multiple organs or tissues, including the skin, blood and nervous system. Compared with non-paraneoplastic autoimmune diseases, PAD have different aetiologies, pathologies, disease symptoms and treatment responses. There are two main origins of autoimmunity in PAD: neoplasm-mediated dysregulated homeostasis in immune cells/organs and in autoantigens. Pathologically, PAD are mediated predominantly by either autoantibodies or autoreactive T-cells. In the past decade, significant progress has been achieved in increasing our understanding of the aetiology and pathology of PAD. In this review article, we aim to provide a comprehensive overview of the recent advances in this field.