A novel variant of Chlamydia psittaci causing human psittacosis in China.

From January 2022 to November 2022, sporadic psittacosis occurred in Lishui city, China. The patients were presented with fever, cough, and pulmonary infiltration. Their clinical symptoms were not relieved after receiving cephalosporin, penicillin, beta-lactamase inhibitors, and quinolones. Metagenomic next-generation sequencing of bronchoalveolar lavage fluid samples from the patients revealed Chlamydia psittaci infection. Then, three C. psittaci strains were isolated from the patients. Their whole genome sequences (WGSs) were obtained, and a core genome multilocus sequence typing (cgMLST) method was developed to study the population structure of C. psittaci. Using the constructed cgMLST method, 72 WGSs were divided into four related groups and ten sub-clusters. The Lishui strains formed a unique population of C. psittaci, which might represent a new variant of C. psittaci. In vitro antimicrobial susceptibility testing suggested that the Lishui strains were sensitive to tetracycline, macrolides, quinolones, and no drug-resistance was observed.

WTAP-mediated N6-methyladenine Modification of circEEF2 Promotes Lung Adenocarcinoma Tumorigenesis by Stabilizing CANT1 in an IGF2BP2-dependent Manner.

N6-methyladenosine (m6A) is a common posttranscriptional RNA modification and plays an important role in cancer biology. Circular RNAs (circRNAs) are also reported to participate in lung adenocarcinoma (LUAD) progression. Here, we aimed to investigate the functions of Wilms tumor 1-associating protein (WTAP) methyltransferase and circEEF2 in LUAD cell tumorigenesis, and probe whether circEEF2 functioned through WTAP-induced m6A modification and its potential mechanisms. Functional analyses were conducted by tube formation, sphere formation, 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, and transwell assays in vitro as well as tumor formation experiments in mice, respectively. The N6-methyladenine (m6A) modification in circEEF2 mRNA was determined by RNA immunoprecipitation (Me-RIP) assay. The interaction between IGF2BP2 (Insulin Like Growth Factor 2 MRNA-Binding Protein 2) and circEEF2 or Calcium-activated nucleotidase 1 (CANT1) mRNA was confirmed using RIP assay. LUAD tissues and cells showed high circEEF2 expression, and the deficiency of circEEF2 suppressed LUAD cell angiogenesis, stemness, proliferation, migration, and invasion. WTAP induced circEEF2 m6A modification. WTAP silencing repressed the oncogenic phenotypes of LUAD cells via stabilizing circEEF2 in an m6A-dependent manner. IGF2BP2 interacted with circEEF2 and CANT1, and WTAP and circEEF2 could regulate CANT1 expression through IGF2BP2. The inhibition of LUAD cell oncogenic phenotypes caused by circEEF2 deficiency was abolished by CANT1 overexpression. In addition, WTAP silencing impeded LUAD growth via modulating circEEF2 and CANT1 in vivo. WTAP-mediated m6A modification of circEEF2 promotes lung adenocarcinoma growth and tumorigenesis by stabilizing CANT1 through IGF2BP2.

CBX8 Promotes Epithelial-mesenchymal Transition, Migration, and Invasion of Lung Cancer through Wnt/ß-catenin Signaling Pathway.

BACKGROUND: Lung cancer (LC) is primarily responsible for cancer-related deaths worldwide. Epithelial-mesenchymal transition (EMT) is a process in which epithelial cells acquire mesenchymal features and is associated with the development of tumors. CBX8, a member of the PcG protein family, plays a critical role in various cancers, containing LC. However, specific regulatory mechanisms of CBX8 in LC progression are not fully understood. This study aimed to investigate the regulatory role of CBX8 in LC progression. METHODS: Bioinformatics was used to analyze the relationship between CBX8 level and tumor and the enrichment pathway of CBX8 enrichment. qRT-PCR was used to detect the differential expression of CBX8 in LC cells and normal lung epithelial cells. The effects of knockdown or overexpression of CBX8 on the proliferation, migration and invasion of LC cells were evaluated by CCK- -8 assay and Transwell assay, and the levels of proteins associated with the EMT pathway and Wnt/ ß-catenin signaling pathway were detected by western blot. RESULTS: Bioinformatics analysis revealed that CBX8 was highly expressed in LC and enriched on the Wnt/ß-catenin signaling pathway. The expression level of CBX8 was significantly elevated in LC cells. Knockdown of CBX8 significantly inhibited cell proliferation, migration and invasion, and decreased the expression levels of EMT-related proteins and Wnt/ß-catenin pathway-related proteins. Conversely, overexpression of CBX8 promoted cell proliferation, migration and invasion, and increased the expression levels of EMT-related proteins and Wnt/ß-catenin pathway-related proteins. The Wnt inhibitor IWP-4 alleviated the effects produced by overexpression of CBX8. CONCLUSION: Collectively, these data demonstrated that CBX8 induced EMT through Wnt/ß-- catenin signaling, driving migration and invasion of LC cells.

Luteolin suppresses lung cancer progression through targeting the circ_0000190/miR-130a-3p/notch-1 signaling pathway.

Lung cancer is the leading cause of cancer mortality worldwide. Luteolin has been reported to repress the development of lung cancer. And circular RNAs (circRNAs) circ_0000190 was upregulated in lung cancer tissues. This study is designed to explore the roles of luteolin and circ_0000190 in lung cancer progression. Cell viability, colony number, migration, invasion, and apoptosis were detected by Cell Counting Kit-8 (CCK-8), colony formation, transwell, and flow cytometry assays, severally. The lactate dehydrogenase (LDH) release was determined by special kits. Protein levels of B-celllymphoma-2 (Bcl-2) Cleaved-caspase3 (casp3), Bcl-2 related X protein (Bax), Notch-1, hairy enhance of split-1(Hes-1), and vascular endothelium growth factor (VEGF) were determined by western blot assay. Circ_0000190 andmicroRNA-130a-3p (miR-130a-3p) expression were measured by real-time quantitative polymerase chain reaction (RT-qPCR). The binding relationship between circ_0000190 andmiR-130a-3pwas predicted by starbase and then verified by a dual-luciferase reporter and RNA pull-down assays. The biological roles of Luteolin and circ_0000190 on tumor growth of lung cancer were examined by the xenograft tumor model in vivo. Luteolin inhibited cell viability, colony formation, migration, invasion, and promoted apoptosis of lung cancer cells. Moreover, overexpression of circ_0000190 could counteract the suppression role of luteolin on lung cancer development. Andcirc_0000190 directly bound with miR-130a-3p. Luteolin blocked lung cancer cell growth, metastasis, and Notch-1 signaling pathway by modulating the circ_0000190/miR-130a-3pin vitro. Luteolin repressed tumor growth of lung cancer in vivo by regulating circ_0000190. Luteolin dampened the progression of lung cancer partly by regulating circ_0000190/miR-130a-3p, providing an underlying therapeutic target for lung cancer.

Pemetrexed-based first-line chemotherapy had particularly prominent objective response rate for advanced NSCLC: A network meta-analysis.

OBJECTIVE: The aim of the present work was to investigate the clinical efficacy of first-line chemotherapy regimens in the treatment of advanced non-small cell lung cancer (NSCLC) through a comprehensive network meta-analysis (NMA). METHODS: The prospective randomized controlled clinical trials relevant to 10 first-line chemotherapy regimens in the treatment of advanced NSCLC were systematic electronic search in the databases of Pubmed, Embase, Cochrane Library and CNKI. The combined direct or indirect objective response rate (ORR) between each of the 10 first-line chemotherapy regimens was calculated. RESULTS: Seventeen prospective clinical trials of first-line chemotherapy regimens in treatment of advanced NSCLC were included in the NMA. The 10 treatment regimens including A = cisplatin + gemcitabine, B = carboplatin + gemcitabine, C = gemcitabine, D = carboplatin + paclitaxel, E = paclitaxel + gemcitabine, F = docetaxel + carboplatin, G = gemcitabine + vinorelbine, H = pemetrexed + carboplatin, I = cisplatin + pemetrexed and J = cisplatin + docetaxel were compared in the present NMA. Direct pooled results indicated that the ORR was not statistically different (P all > 0.05). However, NMA showed that the combined ORR for regimens A (OR = 1.47, 95% CI: 0.80-2.81), B (OR = 3.22, 95% CI: 1.45-6.923), D (OR = 3.30, 95% CI: 1.22-9.33), E (OR = 4.36, 95% CI: 1.64-12.82), G (OR = 3.72, 95% CI: 1.12-12.83) and I (OR = 5.80, 95% CI: 2.04-17.86) was superior to regimen C. Rank probability analysis indicated that regimen C = gemcitabine and regimen I = cisplatin + pemetrexed had the highest probability of inferior and superior treatment ORR among the 10 first-line chemotherapy regimens. CONCLUSION: Cisplatin + pemetrexed may have particularly prominent ORR for advanced NSCLC as the first-line chemotherapy regimen.