Background: Limited evidence exists on the incidence of gastric cancer (GC), and contradictory results exist for the prognosis of GC based on the Lauren classification. We analyzed the incidence and survival of GC based on the Lauren classification. Methods: The Surveillance, Epidemiology, and End Results (SEER) database from 1975 through 2015 was used to identify all patients with surgically resected, histologically diagnosed intestinal or diffused-type GC. Propensity score matching was used to analyze the association between the Lauren classification type and prognosis. Results: The trend of total GC incidence showed an obvious decrease (APC = −1.51, 95% CI: −2.31 to −1.01) as well as that of the intestinal type (APC = −1.43, 95% CI: −2.01 to −1.12). However, we found that the relative incidence of the diffused type was increased (APC = 0.6, 95% CI: 0.41–0.82). The trend of the total incidence of GC (APC = −1.31, 95% CI: −1.91 to −1.03) and that of the intestinal type (APC = −1.11, 95% CI: −1.53 to −0.98) was decreased in 40–49-year-olds, but that of the diffused type was increased (APC = 1.5, 95% CI: 1.2–1.72). We found that trends in GC incidence exhibited a similar pattern in the regional and distant stages and showed a decrease from 1975 through 2015. However, the incidence rate of the local stage was increased, with an APC of 0.5 (95% CI: 0.3–0.7). We identified 15,989 GC cases from the SEER database, including 13,852 intestinal-type and 2,138 diffused-type cases. The 1,336 intestinal-type cases were matched with 1,336 diffused-type cases using propensity score matching (PSM), and patients with the diffused type had a better prognosis than patients with the intestinal type (HR = 0.56, 95% CI: 0.45–0.78). However, we found that patients with diffused-type GC had worse survival than patients with intestinal-type GC in the cohort from Renji Hospital (P < 0.001). Conclusion: The total incidence of GC and that of the intestinal-type GC decreased, but the incidence of diffused-type GC increased in 40–49-year-olds. Diffused types of GCs may have a different prognosis compared to intestinal-type GCs in different patient cohorts. Nevertheless, these results should be interpreted with caution in assessing the prognosis in combination with other factors.

Colorectal cancer (CRC) is the third most common cancer worldwide. Several studies have suggested that taraxasterol acetate (TA) can inhibit the growth of tumor cells. However, to date, it remains unclear how TA inhibits cell growth and how RNF31 functions as an oncogene. We examined the expression of RNF31 in CRC tissue samples via immunohistochemistry and elucidated the function of RNF31 in CRC cells by constructing a cell model with RNF31 depletion. A cycloheximide (CHX)-chase analysis and immunofluorescence assays were conducted to demonstrate that TA can promote RNF31 degradation by activating autophagy. We used the PharmMapper website to predict targets of TA and identified RNF31. CHX-chase experiments showed that TA could facilitate RNF31 degradation, which was inhibited by the administration of chloroquine. Immunofluorescence assays showed that RNF31 protein was colocalized with LC3I/II and p62, suggesting that TA promoted RNF31 degradation by activating autophagy. We also found that CRC patients with RNF31 overexpression had poorer survival than those with low RNF31 expression. The results of the CHX-chase experiment showed that depletion of RNF31 alleviated p53 degradation, which was inhibited by MG132. A series of co-immunoprecipitation (Co-IP) assays revealed that RNF31 interacts with p53 and promotes p53 ubiquitination and degradation. A Co-IP assay performed with a truncated RNF31 plasmid showed that the PUB domain interacts with p53. Moreover, the PUB domain is the key structure in the induction of p53 ubiquitination. Our findings reveal a key role of RNF31 in CRC cell growth and indicate a mechanism through which TA inhibits cell growth.

Colorectal cancer (CRC) is a tumor that derives from the rectum or colon, and colon adenocarcinoma (COAD) is the most common type of CRC. The present study was performed to identify genes that serve critical roles in the survival of patients with COAD. RNA‑sequencing data of COAD was extracted from The Cancer Genome Atlas database, which included 480 tumor samples and 41 normal samples. Using the limma package, differential expression analysis was performed to identify the differentially expressed genes (DEGs). In addition, the potential functions and pathways for the identified DEGs were analyzed using the clusterProfiler package. After the samples were divided into high and low expression groups, survival analysis for the two groups was performed using the Kaplan‑Meier model. Using Cytoscape software, a protein‑protein interaction network was generated for the survival‑associated genes. A total of 1,519 DEGs, including 568 upregulated genes and 951 downregulated genes, were identified in the COAD samples. Enrichment analysis suggested that the DEGs were implicated in numerous functional terms and pathways. Furthermore, 109 DEGs were identified to be survival‑associated genes in COAD. According to the degrees of the network nodes, 5‑hydroxytryptamine receptor 1D (HTR1D), TIMP metallopeptidase inhibitor 1 (TIMP1), serpin family E member 1 (SERPINE1), matrix metallopeptidase 3 (MMP3) and cannabinoid receptor 2 (CNR2) were key nodes, and the expression levels of these genes were analyzed in clinical samples of CRC. Therefore, the results of the present study suggest HTR1D, TIMP1, SERPINE1, MMP3 and CNR2 may affect the prognosis of patients with COAD.

Outcomes of endoscopic sphincterotomy vs open choledochotomy for common bile duct stones