microRNA-486-5p Regulates DNA Damage Inhibition and Cisplatin Resistance in Lung Adenocarcinoma by Targeting AURKB.

Lung adenocarcinoma (LUAD) severely affects human health, and cisplatin (DDP) resistance is the main obstacle in LUAD treatment, the mechanism of which is unknown. Bioinformatics methods were utilized to predict expression and related pathways of AURKB in LUAD tissues, as well as the upstream regulated microRNAs. qRT-PCR assayed expression of AURKB and microRNA-486-5p. RIP and dual-luciferase experiments verified the binding and interaction between the two genes. CCK-8 was used to detect cell proliferation ability and IC50 values. Flow cytometry was utilized to assess the cell cycle. Comet assay and western blot tested DNA damage and γ-H2AX protein expression, respectively. In LUAD, AURKB was upregulated, but microRNA-486-5p was downregulated. The targeted relationship between the two was confirmed by RIP and dual-luciferase experiments. Cell experiments showed that AURKB knock-down inhibited cell proliferation, reduced IC50 values, induced cell cycle arrest, and caused DNA damage. The rescue experiment presented that high expression of microRNA-486-5p could weaken the impact of AURKB overexpression on LUAD cell behavior and DDP resistance. microRNA-486-5p regulated DNA damage to inhibit DDP resistance in LUAD by targeting AURKB, implying that microRNA-486-5p/AURKB axis may be a possible therapeutic target for DDP resistance in LUAD patients.

Methanogenic pathway and microbial succession during start-up and stabilization of thermophilic food waste anaerobic digestion with biochar.

One of the major obstacles for thermophilic anaerobic digestion is the process instability during start-up. This study proposed the use of a cost-effective additive, biochar, to accelerate and stabilize the start-up of thermophilic semi-continuous food waste anaerobic digestion. The results showed that the reactors with biochar addition resulted in up to 18% higher methane yield as compared to the control reactors (without biochar). The key microbial networks were elucidated through thermochemical and microbial analysis. Particularly, the addition of biochar promoted the growth of electroactive Clostridia and other electroactive bacteria, while the absence of biochar promoted the growth of homoacetogenic Clostridia and syntrophic acetate oxidizing bacteria. It was revealed that biochar promoted direct interspecies electron transfer between the microbes and was responsible for the faster degradation of volatile fatty acids. Furthermore, reactors with biochar also enhanced the thermodynamically favourable acetoclastic methanogenic pathway due to the higher abundance of Methanosarcina.

The Role of Cavin3 in the Progression of Lung Cancer and Its Mechanism.

OBJECTIVE: The purpose of this study was to describe the role of Cavin3 in the progression of lung cancer and its underlying mechanism. METHODS: Totally, 200 cases of lung cancer tissues and corresponding paracancer tissues were collected. Cavin3 expression in samples was determined by qRT-PCR, and the correlation with lung cancer stages as well as prognosis was statistically analyzed combined with matched clinical information. To investigate the mechanism of Cavin3 in lung cancer progression, firstly, Cavin3 was detected in lung cancer cell lines A549, PC9, and H520. Then, cells with stable Cavin3 overexpression and Cavin3 knockout were established to determine the effect of Cavin3 overexpression on the mammalian target of rapamycin (mTOR) signaling pathway. Subsequently, cells were harvested for cell proliferation, migration, and invasion assays in vitro, as well as nude mouse transplantation tumor experiment in vivo. RESULTS: Cavin3 was seen to be highly expressed in cancer tissues. Statistical analysis with matched clinical data showed that Cavin3 as a prognostic indicator of lung cancer had important clinical value. In addition, it could be found that high expression of Cavin3 was able to promote cell proliferation, migration, and invasion and also potentiate tumor formation in vivo. CONCLUSION: Cavin3 was highly expressed in lung cancer, and it was capable to promote cell proliferation, invasion, and migration.

The Effects of Serum hs-CRP on the Incidence of Lung Cancer in Male Patients with Pulmonary Tuberculosis.

BACKGROUND: This study intended to investigate the effects of serum high-sensitivity C-reactive protein (hs-CRP) on the incidence of lung cancer in male patients with pulmonary tuberculosis. METHODS: A total of 1091 male patients with pulmonary tuberculosis in Zhejiang Cancer Hospital, Hangzhou, China from Jan 2009 to Jan 2012 were selected as the research objects. All patients were followed up from the beginning of hospitalization. According to serum hs-CRP level, patients were divided into two groups: group A (hs-CRP < 1 mg/L) and group B (hs-CRP > 3 mg/L). The relationship between baseline hs-CRP and the risk of lung cancer in patients with pulmonary tuberculosis was analyzed by multivariate Cox proportional risk regression model, and the serum levels of hs-CRP between lung cancer patients in all groups and other non-lung cancer patients were compared. RESULTS: There were differences in age, drinking, smoking, diabetes history, body mass index (BMI), thyroglobulin (TG), history of hypertension and hyperglycemia among the three groups (P=0.036, 0.018, 0.040, 0.029, 0.006, 0.034, 0.020, 0.010). The serum levels of hs-CRP in patients with squamous carcinoma, adenocarcinoma and small cell carcinoma were significantly higher than those in non-lung cancer patients (P=0.022, 0.043, 0.011). The incidence rates of lung cancer in patients in group B and C were 1.37 and 1.69 times higher than that in group A, respectively. CONCLUSION: The increased serum level of hs-CRP will increase the incidence rate of lung cancer in male patients with pulmonary tuberculosis.

miR-21 promotes non-small cell lung cancer cells growth by regulating fatty acid metabolism.

BACKGROUND: Lung cancer is one of the most common malignant tumors worldwide. CD36 is a receptor for fatty acids and plays an important role in regulating fatty acid metabolism, which is closely related to tumorigenesis and development. The regulation of miR-21 and its role in tumorigenesis have been extensively studied in recent years. However, the relationship between miR-21 and CD36 regulated fatty acid metabolism in human non-small cell lung cancer remains unknown. METHODS: In this study, lentivirus transfection, qRT-PCR, cell migration, immunofluorescence, and western blot were used to examine the relationship between miR-21 and CD36 regulated fatty acid metabolism and the regulation role of miR-21 in human non-small cell lung cancer. RESULTS: This study demonstrated that up-regulation of miR-21 promoted cell migration and cell growth in human non-small cell lung cancer cells. Moreover, the intracellular contents of lipids including cellular content of phospholipids, neutral lipids content, cellular content of triglycerides were significantly increased following miR-21 mimic treatment compared with control, and the levels of key lipid metabolic enzymes FASN, ACC1 and FABP5 were obviously enhanced in human non-small cell lung cancer cells. Furthermore, down-regulation of CD36 suppressed miR-21 regulated cell growth, migration and intracellular contents of lipids in human non-small cell lung cancer cells, which suggested that miR-21 promoted cell growth and migration of human non-small cell lung cancer cells through CD36 mediated fatty acid metabolism. Inhibition of miR-21 was revealed to inhibit cell growth, migration, intracellular contents of lipids, and CD36 protein expression level in human non-small cell lung cancer cells. In addition, PPARGC1B was a direct target of miR-21, and down-regulation of PPARGC1B reversed the inhibition of CD36 expression induced by miR-21 inhibitor. CONCLUSIONS: These results explored the mechanism of miR-21 promoted non-small cell lung cancer and might provide a novel therapeutic method in treating non-small cell lung cancer in clinic.

Expression of Chemokine XCL2 and CX3CL1 in Lung Cancer.

BACKGROUND Chemokines are a family of small proteins secreted by cells with chemotactic activity, and they play important roles in cell adhesion. However, the expression of chemokine XCL2 and CX3CL1 in lung cancers in different pathological stages remains unclear. MATERIAL AND METHODS XCL2 and CX3CL1 expression in lung cancers and adjacent non-cancerous tissues was detected by quantitative PCR and ELISA. The relative expression of both chemokines in lung cancers in different pathological stages was compared by immunohistochemical assay. RESULTS The relative expression level of XCL2 and CX3CL1 in lung cancer was significantly higher compared with adjacent normal tissues (P<0.001). The expression level of both chemokines was significantly increased with higher pathological stages, as indicated by immunohistochemical assay (P<0.05 or P <0.001). Their expression level in cancers with higher numbers of metastatic lymph nodes was also significantly increased compared with cancers with lower numbers of metastatic lymph nodes (P<0.05 or P<0.001). CONCLUSIONS The expression of XCL2 and CX3CL1 increases with increasing degree of malignancy, indicating that both chemokines might be important targets in gene therapy for lung cancer.

[Follow-up of twelve cases of heart transplantation].

OBJECTIVE: To observe the effects of heart transplantation. METHODS: Twelve patients undergoing orthotopic heart transplantation, one of which underwent combined heart and kidney transplantation (HKT), from June 1997 to June 2002 were followed up to observe the complications, work ability, life quality and psychic status. RESULTS: One of the 12 patients died of acute rejection and one died of acute renal failure during perioperative period. Ten cases (83.3%) survived the operation. Then one of the 10 patients died of acute rejection due to stopping Cellcept 7 months after operation; and the other 9 patients had lived well for 1 to 9 years, of which one recipient undergoing HKT survived for nearly 3 years. One year after operation the 9 patients showed class I heart function (NYHA), and all resumed their original work. One patient suffered from schizophrenia 1 week after operation. After the operation every year all cases were to receive coronary angiography with the results showing thinner coronary artery and less lateral branches, and myocardium, emission computed tomography (ECT) scanning that revealed local ischemia in anterior or posterior myocardium in 2 cases 4 and 5 years after respectively, however, no symptom of coronary artery disease was seen in all patients. Two cases, including the one receiving HKT, had symptoms of diabetes mellitus. Two patients thoracotomy during the perioperative period because of cardiac tamponade or too much blood drainage. All cases suffered from right heart failure, mouth ulcer and hypertension due to taking CsA and they had to take antihypertension drug to control their blood pressure. No malignant tumor had been found. CONCLUSION: Heart transplantation is an effective treatment for end-stage dilated cardiomyopathy. But many complications may follow. Some of them may endanger patients' life, and others may affect the quality of life. To trace the patients closely and deal with various complications in time will improve the effect of cardiac transplantation.