Background: Colon cancer is one of most malignant cancers around worldwide. Nearly 20% patients were diagnosed at colon cancer with metastasis. However, the lack of understanding regarding its pathogenesis brings difficulties to study it.Methods: In this study, we acquired high‐sequence data from GEO dataset, and performed integrated bioinformatic analysis including differently expressed genes, gene ontology and Kyoto Encyclopedia of Genes and Genomes pathways analysis, protein–protein analysis, survival analysis to analyze the development of colon cancer.Results: By comparing the colon cancer tissues with normal colon tissues, 109 genes were dysregulated; among them, 83 genes were downregulated and 26 genes were upregulated. Two clusters were founded based on the STRING database and MCODE plugin of cytoscape software. Then, six genes with prognostic value were filtered out in UALCAN website.Conclusion: We found that SPP1, VIP, COL11A1, CA2, ADAM12, INHBA could provide great significant prognostic value for colon cancer.

Older patients who are diagnosed with colon cancer face unique challenges, specifically regarding to cancer treatment. The aim of this study was to identify prognostic signatures to predicting prognosis in colon cancer patients through a detailed transcriptomic analysis. RNA-seq expression profile, miRNA expression profile, and clinical phenotype information of all the samples of TCGA colon adenocarcinoma were downloaded and differentially expressed mRNAs (DEMs), differentially expressed lncRNAs (DELs) and differentially expressed miRNAs (DEMis) were identified. A competing endogenous RNA (ceRNA) network was constructed further and DEMs related with prognosis in the ceRNA network was screened using Cox regression analysis. Risk score models for predicting the prognosis of colon cancer patients were built using these DEMs. A total of 1476 DEMs, 9 DELs, and 243 DEMis between the tumor and normal samples were identified and functional enrichment analyses showed that the DEMs were significantly enriched in the nervous system development, ribosome biogenesis pathways in eukaryotes, and drug metabolism cytochrome P450. Twelve DEMs related with prognosis were screened from the ceRNA network. Thereafter, the risk score models of prognostic DEMs were obtained, involving seven DEMs (SGCG, CLDN23, SLC4A4, CCDC78, SLC17A7, OTOP3, and SMPDL3A). Additionally, cancer stage was identified as a prognostic clinical factor. This prognostic signature was further validated in two independent datasets. Our study developed a seven-mRNA and one-clinical factor signature that are associated with prognosis in colon cancer patients, which may serve as possible biomarkers and therapeutic targets in the future.

Objective. Ulcerative colitis (UC) is a chronic idiopathic inflammatory bowel disease whose treatment strategies remain unsatisfactory. This study aims to investigate the mechanisms of Quyushengxin formula acting on UC based on network pharmacology.Methods. Ingredients of the main herbs in Quyushengxin formula were retrieved from the Traditional Chinese Medicine Systems Pharmacology (TCMSP) database. Absorption, distribution, metabolism, and excretion properties of all ingredients were evaluated for screening out candidate bioactive compounds in Quyushengxin formula. Weighted ensemble similarity algorithm was applied for predicting direct targets of bioactive ingredients. Functional enrichment analyses were performed for the targets. In addition, compound-target network, target-disease network, and target-pathway network were established via Cytoscape 3.6.0 software.Results. A total of 41 bioactive compounds in Quyushengxin formula were selected out from the TCMSP database. These bioactive compounds were predicted to target 94 potential proteins by weighted ensemble similarity algorithm. Functional analysis suggested these targets were closely related with inflammatory- and immune-related biological progresses. Furthermore, the results of compound-target network, target-disease network, and target-pathway network indicated that the therapeutic effects of Quyushengxin on UC may be achieved through the synergistic and additive effects.Conclusion. Quyushengxin may act on immune and inflammation-related targets to suppress UC progression in a synergistic and additive manner.

Background. Ulcerative colitis (UC) is a chronic inflammatory disease that affects the colon and the rectum. Recently, some studies have shown that microorganisms in the gut play important roles in many chronic diseases such as UC. Methods. To study the candidate viruses and bacteria involved in UC and to investigate the therapeutic mechanism of Quyushengxin formula (QYSX) in UC patients, metagenomic sequencing was performed on the feces from healthy donors and UC patients before and after QYSX treatment. Results. QYSX improved the symptoms of UC. In all participants, Caudovirales and Herpesvirales were the most dominant viruses. The abundance of Caudovirales in UC patients was significantly higher than that in the normal controls, while QYSX restored Caudovirales abundance. Furthermore, the abundance of crAssphage was enhanced in UC patients compared with the normal control, while the diversity was then decreased after QYSX treatment. However, there was no significant difference (P > 0.05). Additionally, other non‐crAssphage bacteriophages including phiST, SP-10, and phi17:2 were higher in UC patients and QYSX decreased these viruses, while the trends of MED4−213, P-HM1, and P−HM2 were adverse. Interestingly, PhiDP23.1 was only found in UC patients before and after QYSX treatment. In addition, Bifidobacterium, Bacteroidetes, Prevotellaceae, Actinobacteria, and Corynebacteriales were the biomarkers in UC patients after QYSX treatment due to their high abundance. GO terms and KEGG analysis showed that the identified gut microbiome was involved in many biological processes and pathways. Conclusions. QYSX could regulate disordered gut microbiome and phages, indicating that QYSX has great therapeutic potential for UC.

Purpose. To study the therapeutic effect of Quyu (QY) Shengxin (SX) decoction (QYSXD) in mice with dextran sulfate sodium- (DSS-) induced ulcerative colitis and to investigate the effects of QYSXD on the regulation of the receptor-interacting protein kinase 1 (RIP1)/receptor-interacting protein kinase 3 (RIP3)/nucleotide-binding oligomerization domain-like receptor family pyrin domain protein 3 (NLRP3) signaling pathway. Method. Thirty-six mice were randomly divided into the following 6 groups: the experimental group (QYSX group), the model group (DSS group), the positive control group (5-aminosalicylic acid (5-ASA) group), the control group, the first component group (QY group), and the second component group (SX group). Each group included 6 mice. Ulcerative colitis (UC) was induced in the mice by providing 3.5% DSS in drinking water. The mice were weighed every day to evaluate the disease activity index (DAI). After 7 days, the mice were sacrificed, and colonic tissues were obtained for colon length measurement. The morphological changes in the colon and the pathological scores of the mice in each group were observed by hematoxylin-eosin (HE) staining. The messenger ribonucleic acid (mRNA) and protein expression levels of RIP1, RIP3, dynamin-related protein 1 (Drp1), NLRP3, cysteinyl aspartate specific proteinase-1 (caspase-1), interleukin (IL)-1β, and IL-18 in the colon tissues of the mice in each group were detected and compared by real-time quantitative reverse transcription PCR (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA). The levels of RIP1, RIP3, NLRP3, IL-1β, and IL-8 in the colonic mucosa were detected by ELISA. Western blotting was used to compare the protein expression of Drp1, caspase-1, mitochondrial fission protein 1 (FIS1), and mitophagy-associated protein light chain 3a/b (LC3a/b) among groups. The levels of reactive oxygen species (ROS) in the colonic mucosal cells were compared by immunofluorescence. Results. Compared with those in the DSS group, the mice with DSS-induced colitis in the QYSX group exhibited clearly higher body weights ( ) and DAI scores ( ). The colon lengths of the mice in the QYSX group were longer than those in the DSS group ( ), and the pathological score of the QYSX group was lower than that of the DSS group ( ). The RIP1, RIP3, Drp1, IL-1β, IL-18, and caspase-1 mRNA levels in the QYSX, 5-ASA, SX, and QY groups were significantly lower than those in the DSS group ( ), but there were no differences between the QYSX group and the 5-ASA group. The levels of RIP1, RIP3, NLRP3, IL-1β, and IL-18 in the QYSX group were lower than those in the DSS group ( ). The levels of Drp1, caspase-1, FIS1, and LC3a/b in the QYSX group and the 5-ASA group were lower than those in the DSS group ( ). The levels of ROS in the colonic mucosal cells in the QYSX, 5-ASA, and QY groups were lower than those in the DSS group ( ). Conclusion. QYSXD has certain therapeutic effects on DSS-induced colitis in mice and may be as effective as 5-ASA. QY and SX decoctions also have certain effects on colitis; however, these decoctions are not as beneficial as QYSXD. QYSXD may ameliorate colitis by inhibiting the expression of RIP1/RIP3/NLRP3 pathway-related proteins and reversing mitochondrial dysfunction to control inflammation.