No abstract

Lung cancer is the most frequent and fatal malignancy in humans worldwide, yet novel successful drugs for control of this disease are still lacking. Ipomoea batatas polysaccharides (IBPs) have been implicated in inhibiting diverse cancer types, but their functions in mitigating lung cancer are largely unknown. In this study, we identify a role of IBP in inhibiting lung cancer proliferation. We found that IBP significantly impedes the proliferation of lung cancer cells by inducing cytostatic macroautophagy both in vitro and in vivo . Mechanistically, IBP specifically promotes ubiquitination-mediated degradation of PAK1 (p21-activated kinase 1) and blocks its downstream Akt1/mTOR signaling pathway, leading to increased autophagic flux. In lung cancer xenografts in mice, IBP-induced cytostatic autophagy suppresses tumor development. Through site-directed mutational analysis, the underlying signaling augments ubiquitination via PAK1-ubiquitin interaction. Collectively, this work unravels the molecular mechanism underpinning IBP-induced cytostatic autophagy in lung cancer and characterizes IBP as a potential therapeutic agent for lung cancer treatment.

Lung cancer remains the leading cancer killer worldwide. Early diagnosis can effectively increase the patient cure rate but existing diagnostic methods limit early lung cancer diagnosis. Therefore, development of a simple but efficient lung cancer screening method is important to improvement of both the diagnosis rate and the survival rate of lung cancer patients. In this study, ten photosensitive materials with high sensitivity and high specificity were screened accurately to construct a microarray sensor that can rapidly identify six types of lung cancer biomarkers in exhaled breath. Results from hierarchical cluster analysis (HCA), principal component analysis (PCA) and difference maps showed that the classification of the analytes agreed with structure similarity laws. The detection results from parallel experiments and structurally similar analytes, in turn, cluster into a group; the fingerprints of the different analytes have specific response regions. The well-screened sensor chip fabrication workload and cost were both reduced by approximately two thirds, while the microfluidic device sensitivity and stability increased by approximately 1.3 times their corresponding values before optimization. The dual-channel device also offers real-time contrast detection and synchronous parallel detection functions and has potential application prospects for use in extensive screening of high-risk populations for lung cancer.

Lung cancer remains the leading cancer killer worldwide.

Background： Tumor-associated macrophages(TAMs), especially M2 macrophages, plays a critical role in Colorectal cancer initiation, promotion, and metastasis. However, the underlying mechanisms still remain unresolved. Methods：The profile of ATAC-seq was employed to detect genes with open chromatin. The RNA-seq was used to identify differentially expressed genes (DEGs) and those DEGs with open chromatin in promoter regions were identified as hub gene. Then, CIBERSORT, quanTIseq and XCELL algorithm were employed to quantified the expression of M2 macrophages and Pearson correlation analysis was used to identified the relationship with M2 macrophages and hub gene. After that, the macrophages profile and scRNA-seq profile were used to identify the gene expression in different phenotype macrophage. GO/KEGG analysis, GSEA, GSVA were used for gene function analysis. Finally, the target gene which promote M2 macrophages polarization were further explored by experiment. Results：In this study, we acquired 15,650 genes with open chromatin in promoter regions and 3,241 genes were identified as differential expression genes with open chromatin. Integrated CIBERSORT, quanTIseq and XCELL algorithm, we identified 72 genes were correlated with M2 macrophages (r>0.2, p<0.05). According to the macrophages profile from GEO database, 2 genes were identified as differential expressed genes which high expressed in M2 macrophages. By applying scRNA-seq, APBB1IP was the only gene expressed in macrophage and high expressed in M2 phenotype. M2 macrophage polarization were inhibited after knockdown of APBB1IP in vitro experiments. Conclusion：APBB1IP, characterized by chromatin accessibility, downregulated in patients with COAD and induced M2 macrophage polarization.