Despite advances in diagnosis and treatment, gastric cancer (GC) remains a refractory disease, which limits overall survival. Therefore, it is key to identify novel targets to develop more effective and precise treatment. Circular RNAs (circRNAs) serve essential roles in the process of various human cancers. Through analyzing GSE83521 dataset, the present study identified a novel circRNA derived from ribosomal protein S19 (circRPS19), which was considered a potential treatment target for GC. Results of RT‑qPCR indicated that circRPS19 was upregulated in GC compared with normal gastric epithelial cells. Loss‑of function assays revealed that silencing of circRPS19 suppressed proliferation and aerobic glycolysis but increased apoptosis of GC cells. circRPS19 upregulated ubiquitin‑specific processing protease 7 (USP7) expression by sponging microRNA (miR)‑125a‑5p. circRPS19 stabilized hexokinase 2 (HK2) protein by USP7‑mediated deubiquitination of HK2. In vivo experiments confirmed that circRPS19 promoted GC progression and aerobic glycolysis. Taken together, circRPS19 induced aerobic glycolysis of GC cells by stabilizing HK2 protein via the miR‑125a‑5p/USP7 axis and thus promoting the progression of GC. These findings suggested that circRPS19 served a critical role in the progression of GC and may be a novel therapeutic target for GC.

Objective: Gastric cancer (GC) remains a leading cause of cancer-related mortality, with poorly cohesive carcinoma (PCC) exhibiting rising incidence and poor therapeutic responses. In this study, we constructed a panel of patient-derived organoids of GC and used them to understand histological accuracy and sensitivity profiles as well as the influence of microenvironment on these special GC subtypes.Methods: A total of 23 patient-derived GC organoid models including 12 PCC and 11 non-poorly cohesive carcinoma (NPCC) were established. Histopathological and genetic fidelity to primary tumors was validated using immunohistochemistry (IHC), immunofluorescence (IF), and H&E staining. Relative growth kinetics between PCC and NPCC organoids were measured and compared. Sizes of subcutaneously xenografted tumors harbored by mice representing different types of GC organoids were analyzed. We further examined drug sensitivities between docetaxel, 5-fuorouracil (5-FU), oxaliplatin, and irinotecan against our collected samples of patient-derived organoids. The impact of cancer-associated fibroblasts (CAFs) on organoid growth and chemoresistance was analyzed via co-culture experiments.Results: Organoids retained genetic and histopathological features of primary tumors. PCC-derived organoids displayed rapid growth characteristics in vitro and produced more rapidly growing tumors in vivo than NPCC. PCC organoids showed heightened sensitivity to docetaxel with lower IC₅₀, but no significant differences were observed for 5-FU, oxaliplatin, or irinotecan. CAF co-culture enhanced organoid proliferation and conferred resistance to all tested chemotherapeutic agents.Conclusion: Patient-derived GC organoids especially PCC subtypes reliably recapitulate the complexity of solid-tumors heterogeneity, predict drug responses, and elucidate stromal contributions to therapy resistance. This model could be used to develop tailoring treatments and improve personalization of therapy for clinical management of PCC.

Background: Chemotherapy, as one of the main treatments for patients with colorectal cancer (CRC), brings clinical benefits with varying degrees of gastrointestinal reactions. Post-chemotherapy diarrhea is one of the factors affecting the quality of life of cancer patients. In severe cases, it can cause interruption of the chemotherapy process and even be life-threatening. Probiotics’ role in preventing post chemotherapy diarrhea in CRC patients has not been proven. Methods: This meta-analysis was registered with PROSPERO (CRD42023480526). A comprehensive search using subject terms and keywords was conducted to identify randomized controlled trials. Six databases, CNKI, Wanfang, VIP Journals, PubMed, EMBASE, and Web of Science, were searched from their inception until January 16, 2024. The search terms used included “cancer,” “tumor,” “chemotherapy,” “diarrhea,” “probiotics,” and “placebo.” Clinical studies using probiotics to intervene in post chemotherapy diarrhea in CRC patients were included and data were independently extracted for each study. Meta-analysis and sensitivity analysis were performed using RevMan 5.4 and Stata 14 software. Results: Eighteen studies involving 1526 patients were included in this analysis. Meta-analysis demonstrated that probiotics significantly reduced the incidence of diarrhea following chemotherapy in the probiotic group compared to the control group (risk ratio, 0.51; 95% confidence interval: [0.40–0.64]; P = .029). Meanwhile, the use of probiotics significantly shortened the duration of diarrhea (risk ratio: -2.38, 95% confidence interval: [-2.96 to 1.80]). Furthermore, probiotics have been shown to positively affect other gastrointestinal symptoms. Specifically, probiotics significantly alleviated bloating, nausea/vomiting, loss of appetite, and abdominal pain. However, no significant differences were observed in the effects of probiotics on enteritis, tumor necrosis factor-α, diamine oxidase, and interleukin-6. Conclusion: The comprehensive analysis of 18 randomized controlled trials provided compelling evidence that the probiotics have significant clinical value in preventing the onset of diarrhea, shortening the duration of diarrhea, and alleviating chemotherapy-induced gastrointestinal symptoms.

BACKGROUND Adipocytes, especially adipocytes within tumor tissue known as cancer-associated adipocytes, have been increasingly recognized for their pivotal role in the tumor microenvironment of gastric cancer (GC). Their influence on tumor progression and patient prognosis has sparked significant interest in recent research. The main objectives of this study were to investigate adipocyte infiltration, assess its correlation with clinical pathological features, develop a prognostic prediction model based on independent prognostic factors, evaluate the impact of adipocytes on immune cell infiltration and tumor invasiveness in GC, and identify and validate genes associated with high adipocyte expression, exploring their potential diagnostic and prognostic value. AIM To explore the relationship between increased adipocytes within tumor tissue and prognosis in GC patients as well as the associated mechanisms and potential biomarkers, using public databases and clinical data. METHODS Using mRNA microarray datasets from the Gene Expression Omnibus database and clinical samples from Jiangsu Provincial Hospital, survival and regression analyses were conducted to determine the relevant prognostic factors in GC. Feature gene selection was performed using least absolute shrinkage and selection operator and support vector machine recursive feature elimination algorithms, followed by differential gene expression analysis, gene ontology, pathway analysis, and Gene Set Enrichment Analysis. Immune cell infiltration was analyzed using the CIBERSORT algorithm. RESULTS Tumor adipocyte infiltration correlated with poor prognosis in GC, leading to the development of a highly accurate and discriminative prognostic prediction model. Key genes, ADH1B , SFRP1 , PLAC9 , and FABP4 , were identified as associated with high adipocyte expression in GC. The diagnostic and prognostic potential of these identified genes was validated using independent datasets. Downregulation of immune cells was observed in GC with high adipocyte expression. CONCLUSION GC with high intratumoral adipocyte expression demonstrated aggressive tumor biology and a poorer prognosis. The genes ADH1B , SFRP1 , PLAC9 , and FABP4 have been identified as holding diagnostic and prognostic significance in GC. These findings strongly support the use of adipocyte expression as a valuable indicator of tumor invasiveness and anticipated patient outcomes in GC.

Background: The identification of reliable biomarkers for predicting disease recurrence and the survival of patients with cancer is of great importance. Numerous previous studies have revealed that the abnormal expression of the suppressor of cytokine signaling 3 (SOCS3) was associated with patient outcomes. However, these results were inconsistent. The aim of the present study was to assess the prognostic value of SOCS3 in patients with solid tumors.Methods: Studies focusing on the prognostic value of SOCS3 in solid tumors were searched for in the PubMed, Embase, Web of Science, and Scopus databases. We included studies that compared disease-free survival (DFS) and overall survival based on different levels of SOCS3. Other outcomes (e.g., Edmondson grading, tumor size, tumor vascular invasion, lymph node invasion, and distant metastasis) were also considered. The hazard ratio (HR)/risk ratio (RR) and corresponding 95% CI were determined.Results: Twelve studies with 1,551 patients were included in this meta-analysis. The pooled analysis demonstrated that the higher expression of SOCS3 was significantly associated with better disease-free survival (HR:0.36, 95% CI:0.17–0.77, P < 0.001) and overall survival (HR:0.45, 95% CI:0.32–0.62, P < 0.001) compared with low expression. Moreover, SOCS3 expression was closely correlated with the Edmondson grading [odds ratio (OR):0.77, 95% CI:0.61–0.98, P = 0.033], vascular invasion (OR:0.63, 95% CI:0.52–0.78, P < 0.001), and distant metastasis (OR:0.73, 95% CI:0.51–1.03, P = 0.076). However, the levels of SOCS3 were not significantly associated with tumor size (OR:0.85, 95% CI:0.71–1.03, P = 0.090) and lymph node invasion (OR:0.73, 95% CI:0.51–1.03, P = 0.076).Conclusion: Increased SOCS3 expression in tumor mass was associated with better DFS and OS, suggesting it might be a novel and reliable biomarker for predicting the risk of cancer recurrence and mortality.

Background and objective: Numerous previous studies have assessed the prognostic role of 18F-fluorodeoxyglucose positron-emission tomography (18F FDG PET) in patients with biliary tract cancer (BTC), but those results were inconsistent. The present study aims to determine the predictive value of 18F FDG PET in BTC patients via a meta-analysis. Methods: The underlying studies related to 18F FDG PET and BTC patients` outcomes were searched and identified in the online databases. The interested parameters include total lesion glycolysis (TLG), metabolic tumor volume (MTV), primary tumor and metastatic lymph node (LN) maximum standardized uptake value (SUVmax), as well as change of SUVmax (ΔSUVmax) during treatment. Overall survival (OS), disease-free survival (DFS), and progression-free survival (PFS) were considered as the primary endpoints. Hazard ratio (HR) and corresponding 95% confidence intervals (CIs) were defined as the effective measure and calculated by a pooled analysis. Publication bias was assessed by funnel plot, Bagg’s and Egger’s tests. Results: Totally, 23 studies involving 1478 patients were included in the present meta-analysis. After a pooled analysis, it revealed that a high SUVmax was significantly associated with a poor OS (HR:2.07, 95%CI: 1.74–2.46, P = 0.000) and DFS (HR: 2.28, 95%CI: 1.53–3.41, P = 0.000). In addition, an increased TLG level contributed to a shorter OS (HR:1.91, 95%CI: 1.26–2.90, P = 0.002) and DFS (HR: 4.34, 95%CI: 1.42–13.27, P = 0.01). Moreover, we confirmed that an elevated MTV was significantly associated with increased mortality (HR:2.04, 95%CI:1.26–3.31, P = 0.004) and disease relapse (HR: 3.88, 95%CI:1.25–12.09, P = 0.019) risks. Besides, the present study uncovered that increased ΔSUVmax could predict poor OS (HR:1.26, 95%CI:1.06–1.50, P = 0.008) instead of PFS (HR: 1.96, 95%CI: 0.82–4.72, P = 0.280). Lastly, we found that LN SUVmax did not link to OS (HR: 1.49, 95%CI: 0.83–2.68, P = 0.178). No obvious publication bias was detected in the present study. Conclusion: 18F FDG PET parameters, including SUVmax, TLG, MTV, and ΔSUVmax, could be applied as convenient and reliable factors for predicting BTC patients` outcomes.