Cardamonin inhibited the invasion and migration of LLC cells.

<p>After incubation with different drugs for 24 h, the cells in the top on the chamber were removed. (A) The cells that had migrated onto the bottom of the chamber were stained with crystal violet and photographed at 200 × magnification. (B) The invaded cells were counted, and the invasive ratio for each group was presented by comparing to the control group. The percentage of the penetrated cells for each group was showed as the bar graph. In the migration assay, a wound was inflicted in the cell layer, and then treated with different drugs for 24 h. (C) The denuded zone was photographed at 100 × magnification. (D) The traveled distance of the different treatment group was expressed as a ratio to the original distance. The migration ratio of each group was showed as the bar graph. The data were presented as the mean ± SD (<i>n</i> = 5). **p < 0.01, compared to the control group.</p

Chemical structure of cardamonin.

<p>Chemical structure of cardamonin.</p

Cardamonin inhibited the tumor growth and lung metastasis of LLC cells in vivo.

<p>After 20 days of treatment, the mice were sacrificed and the tumors were isolated. The number of lung metastasis was determined by counting the number of metastatic nodules on the lung surface. (A) Tumors in different groups. (B) The initiation and growth of tumors were determined by measuring the average tumor volume. (C) Representative lung tissue sections were stained with H&E and photographed at 100 × magnification. (D) The number of lung surface metastases formed by LLC cells in each group. The data were presented as the mean ± SD (<i>n</i> = 6). The control group represents normal C57BL/6 mice without treatment. The model control group represents C57BL/6 mice that injected s.c. with Lewis lung carcinoma cells and treated with physiological saline.**p < 0.01, compared to the control group.</p

Cardamonin inhibited the proliferation of LLC cells.

<p>LLC cells were treated with rapamycin (0.1 μM) and cardamonin (0.1, 1 and 10 μM) for 48 h. The proliferation was analyzed at by MTT method. The cell viability for each group was presented by comparing to the control group. The data were presented as the mean ± SD (<i>n</i> = 6). **p < 0.01, compared to the control group.</p

Effects of cardamonin on the phosphorylation of mTOR, S6K1 and the expression of E-cadherin, Snail.

<p>LLC cells were treated with different drugs for 24 h, and then the total protein was extracted. Analysis of protein expression of mTOR, S6K1, p-mTOR p-S6K1, E-cadherin and Snail was performed by Western Blot method. Expressions of mTOR, p-mTOR, S6K1, p-S6K1, E-cadherin, Snail and actin were showed as the immunoblot band (<i>n</i> = 3).</p

Integrative topological analysis of mass spectrometry data reveals molecular features with clinical relevance in esophageal squamous cell carcinoma

Combining MS-based proteomic data with network and topological features of such network would identify more clinically relevant molecules and meaningfully expand the repertoire of proteins derived from MS analysis. The integrative topological indexes representing 95.96% information of seven individual topological measures of node proteins were calculated within a protein-protein interaction (PPI) network, built using 244 differentially expressed proteins (DEPs) identified by iTRAQ 2D-LC-MS/MS. Compared with DEPs, differentially expressed genes (DEGs) and comprehensive features (CFs), structurally dominant nodes (SDNs) based on integrative topological index distribution produced comparable classification performance in three different clinical settings using five independent gene expression data sets. The signature molecules of SDN-based classifier for distinction of early from late clinical TNM stages were enriched in biological traits of protein synthesis, intracellular localization and ribosome biogenesis, which suggests that ribosome biogenesis represents a promising therapeutic target for treating ESCC. In addition, ITGB1 expression selected exclusively by integrative topological measures correlated with clinical stages and prognosis, which was further validated with two independent cohorts of ESCC samples. Thus the integrative topological analysis of PPI networks proposed in this study provides an alternative approach to identify potential biomarkers and therapeutic targets from MS/MS data with functional insights in ESCC

Selective oxidative protection leads to tissue topological changes orchestrated by macrophage during ulcerative colitis

Abstract Ulcerative colitis is a chronic inflammatory bowel disorder with cellular heterogeneity. To understand the composition and spatial changes of the ulcerative colitis ecosystem, here we use imaging mass cytometry and single-cell RNA sequencing to depict the single-cell landscape of the human colon ecosystem. We find tissue topological changes featured with macrophage disappearance reaction in the ulcerative colitis region, occurring only for tissue-resident macrophages. Reactive oxygen species levels are higher in the ulcerative colitis region, but reactive oxygen species scavenging enzyme SOD2 is barely detected in resident macrophages, resulting in distinct reactive oxygen species vulnerability for inflammatory macrophages and resident macrophages. Inflammatory macrophages replace resident macrophages and cause a spatial shift of TNF production during ulcerative colitis via a cytokine production network formed with T and B cells. Our study suggests components of a mechanism for the observed macrophage disappearance reaction of resident macrophages, providing mechanistic hints for macrophage disappearance reaction in other inflammation or infection situations