it has been reported that mannose exerts antitumour effects against certain types of cancer. The present study was designed to evaluate whether mannose exerted potential anticancer effects on a549 and H1299 non-small cell lung cancer (nSclc) cells in vitro, which has not been reported previously. a cell counting Kit-8 cell viability assay was used to assess the antiproliferative effects of mannose on nSclc cells. Flow cytometry-based methods were used to evaluate the effects of mannose on the cell cycle distribution and cisplatin-mediated apoptosis of nSclc cells. Transwell migration and invasion assays were conducted to examine whether mannose could inhibit the invasive abilities of nSclc cells. The effects of mannose on the Pi3K/aKT and erK signalling pathways were explored through western blot analysis assessing the expression of phosphorylated (p)-aKT and p-erK1/2. it was found that mannose showed potential anticancer effects against nSclc cells in vitro by inhibiting proliferation, inducing G0/G1 cell cycle arrest, promoting cisplatin-induced apoptosis and decreasing the invasive abilities. These data indicate the potential anticancer properties of mannose and suggest the application of mannose-based therapies to treat nSclc. Cell Counting Kit-8 (CCK-8) assay. cell viability was detected with a ccK-8 assay (dojindo Molecular Technologies, inc.) according to the manufacturer's protocol. cancer cells
The results of this preliminary study suggest that increased levels of CTLA-4 correlate with MPE, and that CTLA-4 may have some diagnostic usefulness when used in combination with conventional tumor markers such as CEA and CYFRA 21-1. These results justify larger, more rigorous studies to validate our findings.
Background and Objective: The incidence of incision infection after lung transplantation is prominently high which affect the prognosis. Summarizing the risk factors related to incision infection after lung transplantation contribute to the control of incision infection by pre-controlling the risk factors. The objective is to summarize risk factors related to wound infection after lung transplantation.Methods: PubMed was used to research the literature relating to the risk factors to incision infection after lung transplantation through 1990 to 2022. The retrieval strategy were Medical Subject Heading (MeSH) terms combined entry terms. Two researchers conducted the literature retrieval independently. Two researchers independently evaluate the quality of the literature and summarize the indicators.
Background: In the treatment of non-small cell lung cancer (NSCLC), recent advances in immunotherapy have heralded a new era. Despite the success of immune therapy, a subset of patients persistently fails to respond. Therefore, to better improve the efficacy of immunotherapy and achieve the purpose of precision therapy, the research and exploration of tumor immunotherapy biomarkers have received much attention.Methods: Single-cell transcriptomic profiling was used to reveal tumor heterogeneity and the microenvironment in NSCLC. The Cell-type Identification by Estimating Relative Subsets of RNA Transcripts (CIBERSORT) algorithm was utilized to speculate the relative fractions of 22 infiltration immunocyte types in NSCLC. Univariate Cox and least absolute shrinkage and selection operator (LASSO) regression analyses were used for the construction of risk prognostic models and predictive nomograms of NSCLC. Spearman's correlation analysis was employed to explore the relationship between risk score and tumor mutation burden (TMB) and immune checkpoint inhibitors (ICIs). Screening of chemotherapeutic agents in the high-and low-risk groups was performed with the "pRRophetic" package in R. Intercellular communication analysis was conducted using the "CellChat" package.Results: We found that most tumor-infiltrating immune cells were T cells and monocytes. We also found that there was a significant difference in the tumor-infiltrating immune cells and ICIs across different molecular subtypes. Further analysis showed that M0 and M1 mononuclear macrophages were significantly different in different molecular subtypes. The risk prediction model was shown to have to ability to accurately predict the prognosis, immune cell infiltration, and chemotherapy efficacy of patients in the high and low-risk groups. Finally, we found that the carcinogenic effect of migration inhibitory factor (MIF) is mediated by binding to CD74, CXCR4, and CD44 receptors involved in MIF cell signaling.
Conclusions:We have revealed the tumor microenvironment (TME) of NSCLC through single-cell data analysis and constructed a prognosis model of macrophage-related genes. These results could provide new therapeutic targets for NSCLC.
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