Background/Aims: Cytokines are key players in tumorigenesis and are potential targets in cancer treatment. Although IL-6 has attracted considerable attention, interleukin 11 (IL-11), another member of the IL-6 family, has long been overlooked, and little is known regarding its specific function in non-small cell lung cancer (NSCLC). In this study, we explored IL-11’s role in NSCLC and the detailed mechanism behind it. Methods: Cell proliferation in response to IL-11 was determined by colony formation, BrdU incorporation and MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) assay. Cell motility was measured by Transwell and wound healing assays. NSCLC xenograft models were used to confirm oncogenic function of IL-11 in vivo. Immunohistochemical staining and western blot assay were performed to detect epithelial–mesenchymal transition (EMT) markers and cell signaling pathway alterations. Eighteen NSCLC patients and 5 normal lung samples were collected together with data from an online database to determine the link between IL-11 expression and malignant progression. Results: We observed that IL-11 was upregulated in NSCLC samples compared with normal tissue samples and correlated with poor prognosis. Data from in vitro and in vivo models indicated that IL-11 promotes cell proliferation and tumorigenesis. Cell migration and invasion were also enhanced by IL-11. Epithelial–mesenchymal transition (EMT) was also observed after IL-11 incubation. Furthermore, IL-11 activated AKT and STAT3 in our experimental models. In addition, we observed that hypoxia induced IL-11 expression in NSCLC cells. Deferoxamine (DFX) or dimethyloxalylglycine (DMOG) induced hypoxia-inducible factor 1-alpha (HIF1α) upregulation, which enhanced IL-11 expression in NSCLC cells. Conclusions: Taken together, our results indicate that IL-11 is an oncogene in NSCLC, and elucidating the mechanism behind it may provide insights for NSCLC treatment.

Purpose In this study, we analyzed the clinical distribution and drug resistance of carbapenem-resistant Klebsiella pneumoniae (CRKP) strains, the minimum inhibitory concentrations (MIC), MIC50 and MIC90, and geographical distribution in Hebei Province, China. We aimed to provide epidemiological research data, formulate appropriate combined treatment schemes, reasonably select antibiotics, and standardize nosocomial infection control schemes. Patients and Methods A total of 6328 strains of CRKP were collected from 2017 to 2019. The MIC was determined for the drug sensitivity test, and the experimental data were statistically analyzed using WHONET5.6. Results The detection rate of CRKP increased annually from 13.4% in 2017 to 14.5% in 2018, and 14.6% in 2019. The ratio of males to females was approximately 2:1; 53.6% were elderly, 39% were adults, 4.8% were minors, and 2.5% were newborns. The specimens collected were mainly sputum (70.9%). The resistance rate of CRKP to carbapenems and other β-lactam antibiotics was found to be increasing, with resistance rates generally greater than 90%. The resistance rate to aminoglycoside antibiotics decreased yearly to approximately 50%, and the resistance rate to quinolones remained unchanged at approximately 80%. From 2017 to 2019, the resistance rate of CRKP in Hebei Province to various antibiotics was high, and the resistance rate to β-lactam antibiotics increased each year. Conclusion The situation of CRKP resistance is severe in Hebei Province, China. The resistance rate to most antibiotics is very high and shows an upward trend. Among them, the resistance rate to polymyxin is low; however, few resistant strains do exist. MIC50 and MIC90 are higher than their MICs. It mainly causes lung infection in elderly men. This study is helpful to improve the diagnosis, treatment, and prevention of CRKP infection in our province.

Background: Ovarian cancer is the most fatal gynecologic malignancy worldwide due to its vagueness, delay in diagnosis, recurrence, and drug resistance. Therefore, a new type of ovarian cancer treatment prediction biomarker is urgently needed to supplement existing tools. A total of 230 people participated in this study. Out of this figure, 100 participants were patients who underwent an ovarian tumor operation, another 100 participants were ovarian benign patients, and the remaining 30 participants were healthy women. Cancer (experimental) group were 100 patients who underwent ovarian tumor operation, while the control groups were 130 participants consisting of 100 ovarian benign patients and 30 healthy women. Levels of SAA, carbohydrate antigen-125 (CA-125), and human epididymis protein 4 (HE4) were assessed using standard laboratory protocols. A total of 5 ovarian cancer tissues and paracancerous tissues were collected and then stored at − 80°C until the qRT-PCR assay was conducted. Results: The ROC curve of SAA concentration in ovarian cancer was plotted to obtain the area under the curve AUC = 0.889, the cutoff value 17.05 mg/L, the sensitivity 78.4% and specificity 86.5%. Compared with pretreatment, the level of serum SAA decreased significantly after treatment. The results revealed that there was a significant correlation between the level of serum SAA and advanced FIGO stage, histology subtype, lymphatic invasion, and distant metastasis (p = 0.003,0.002,0.000 and 0.001). The quantitative Reverse transcription polymerase chain reaction (qRT-PCR) assay revealed that the Messenger RNA (mRNA) of SAA-1 and SAA-4 was much higher in cancer tissues than in adjacent tissues, and MMPs was up-regulation including MMP-1, MMP-9 and MMP-12 in OVCAR-3 cell stimulated by SAA. The transwell assay revealed that SAA could promote OVCAR-3 cell migration. Moreover, SAA can regulate EMT markers and promote AKT pathway activation. Conclusions: In summary, our results demonstrated that SAA may be a potential diagnosis and treatment prediction biomarker. The SAA promotes OVCAR-3 cell migration by regulating MMPs and EMT which may correlate with AKT pathway activation.

To explore serum amyloid A (SAA) and interleukin-6 (IL-6) as potential diagnostic biomarkers for gastric cancer (GCa) and the application value of the combined diagnosis of SAA, IL6, and Cancer embryonic antigen. Serum samples were collected before the initial surgery from 159 patients comprising samples from 122 patients with GCa and 37 patients with benign gastric disease. All patients were hospitalized at Beijing Aerospace General Hospital in China between 2018 and 2020. The IL-6 and SAA levels were assessed using standard laboratory protocols. The levels of SAA and IL-6 were significantly higher in patients with GCa than in controls. Compared with the healthy group, the concentration of SAA and IL-6 in FIGO III-IV group were significantly higher and the difference were statistically significant. In addition, significant differences were observed between the FIGO III-IV group and FIGO I-II groups. The Receiver operating characteristic (ROC) curve for the combined detection of SAA, IL-6, and Cancer embryonic antigen showed an area under the curve (AUC) of 0.948, sensitivity of 91.0%, and specificity of 89.2%. Spearman's correlation analysis indicated obvious correlations among the levels of serum SAA, IL-6, advanced FIGO stage, lymphatic invasion, and distant metastasis. AA and IL-6 may serve as useful biomarkers for poor prognosis of GCa. Clinical diagnosis combined with SAA and IL-6 may help assess therapeutic outcomes.Abbreviations: AUC = area under the curve, CEA = Cancer embryonic antigen, GCa = gastric cancer, IL-6 = Interleukin-6, ROC = receiver operating characteristic, SAA = serum amyloid A.

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