Bacterial vaginosis (BV) is the most common vaginal infection found inwomen in the world. Due to increasing drug-resistance of virulent pathogen such as Gardnerella vaginalis (G. vaginalis), more than half of BV patients suffer recurrence after antibotics treatment. Here, metastable iron sulfides (mFeS) act in a Gram-dependent manner to kill bacteria, with the ability to counteract resistant G. vaginalis for BV treatment. With screening of iron sulfide minerals, metastable Fe 3 S 4 shows suppressive effect on bacterial growth with an order: Gram-variable G. vaginalis >Gram-negative bacteria>> Gram-positive bacteria. Further studies on mechanism of action (MoA) discover that the polysulfide species released from Fe 3 S 4 selectively permeate bacteria with thin wall and subsequently interrupt energy metabolism by inhibiting glucokinase in glycolysis, and is further synergized by simultaneously released ferrous iron that induces bactericidal damage. Such multiple MoAs enable Fe 3 S 4 to counteract G. vaginalis strains with metronidazole-resistance and persisters in biofilm or intracellular vacuole, without developing new drug resistance and killing probiotic bacteria. The Fe 3 S 4 regimens successfully ameliorate BV with resistant G. vaginalis in mouse models and eliminate pathogens from patients suffering BV. Collectively, mFeS represent an antibacterial alternative with distinct MoA able to treat challenged BV and improve women health.
In summary, Oct4 was related to tumor differentiation and later Dukes stage in colon cancer, and was correlated with invasion of lymphatic only in RCC. In addition, Oct4 was a potential prognostic indicator in RCC.
The aim of our study is to investigate the relationship between lymphatic vessel density (LVD) marked by D2-40 and E-cadherin expression and the clinicopathological characteristics of patients with non-small-cell lung cancer (NSCLC). Immunohistochemical analysis was used to detect the expression of D2-40 and E-cadherin in 46 archival surgical specimens of human NSCLC and 10 cases of benign pulmonary disease. The LVD positively stained with D2-40 was observed and counted. The LVD was mainly distributed in the tumor borderline. The LVD in NSCLC tissues was significantly higher than in benign lesions (p < 0.001), and the LVD marked by D2-40 was significantly associated with lymph node metastasis (p < 0.001). The reduced expression of E-cadherin was present in NSCLC tissues. The positive rate of E-cadherin expression was negatively correlated with TNM stage (p = 0.027), pathological grade (p = 0.032), and lymph node metastasis (p = 0.014), and not significantly correlated with histologic classification (p = 0.714) in NSCLC tissues. A correlation analysis showed that high LVD marked by D2-40 was correlated with reduced E-cadherin expression in NSCLC tissues (t = 36.476, p < 0.001). The new monoclonal antibody D2-40 can specifically recognize lymphatic endothelial cells in NSCLC tissue. The relationship between LVD marked by D2-40 and the reduced expression of E-cadherin and lymph node metastasis in NSCLC was demonstrated. The detection of D2-40 and E-cadherin may be used as an indicator of lymph node metastasis in NSCLC.
Purpose Triple-negative breast carcinoma (TNBC) is accompanied with high risk of metastasis and recurrence. The present study aimed to explore the clinicopathological and prognostic roles of putative tumor-related genes in patients with TNBC. Methods Thirty pairs of frozen-thawed tumors were used to select reliable indicators via real-time quantitative polymerase chain reaction (RT-qPCR). Then, 150 pathology specimens were used to evaluate the expression of proteins in TNBC through immunohistochemistry. In addition, Kaplan-Meier curves and Cox regression analysis were also performed to analyze the overall survival and disease-free survival. Results RT-qPCR results indicated that among all the proteins analyzed using fresh-frozen TNBC samples, the expression levels of only Survivin and zinc finger of the cerebellum 1 (ZIC1) were obviously different from those in the corresponding normal tissues. Survivin and ZIC1 expression had opposite effects on the clinicopathological diagnosis and prognostic assessment in TNBC patients. Further, there was a negative correlation between Survivin and ZIC1 expression. In addition, the “Survivin-positive ZIC1-negative group” was associated with histologic grade, lymph node metastasis, and TNM staging ( p < 0.001) and this was also an independent factor for evaluating the prognosis of TNBC in patients. Conclusion In summary, the expression levels of Survivin and ZIC1 in TNBC are different from those in normal tissues and are negatively correlated mutually. The combined detection of Survivin and ZIC1 expression levels could allow better comprehensive diagnosis and prognostic evaluation for TNBC patients.
Artemether, a natural derivative of artemisinin, serves an antitumor role in numerous types of cancer. However, the role and mechanism of action of artemether in hepatocellular carcinoma (HCC) has remained elusive. The present study aimed to investigate whether artemether is able to inhibit the proliferation, invasion and migration of HCC cells by targeting cytochrome P450 family 2 subfamily J member 2 (CYP2J2). Cell Counting Kit-8 (CCK-8) and colony-formation assays were used to examine cell viability. Wound-healing and Transwell assays were used to evaluate the cell invasion and migration ability. The expression levels of the epithelial-mesenchymal transition-related proteins E-cadherin, N-cadherin and vimentin were detected via western blot analysis. To determine the mechanism of the inhibitory effect of artemether on HCC, CYP2J2 was overexpressed and its expression in cells treated with artemether was confirmed using reverse transcription-quantitative PCR and western blot analysis. The effects of artemether on the viability, proliferation and migration of HCC cells overexpressing CYP2J2 were detected using CCK-8, colony-formation, wound-healing and Transwell assays, respectively. Artemether was demonstrated to exert a significant inhibitory effect on the proliferation, invasion and migration of HCC cells. Furthermore, artemether also inhibited CYP2J2 expression in Hep3B2.1-7 cells and CYP2J2 overexpression reversed the inhibitory effect of artemether on the proliferation, invasion and migration of HCC cells. Overall, these results indicated that artemether may inhibit HCC cell proliferation, invasion and migration via targeting CYP2J2.
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