LGALS3 and AXIN1 gene variants playing role in the Wnt/ β-catenin signaling pathway are associated with mucinous component and tumor size in colorectal cancer

Background/Objectives: Gundelia tournefortii (Kenger) is a traditional medicinal plant and exhibits potential anticancer properties. This study investigates the cytotoxic and apoptotic effects of its water extract on human lung carcinoma A549 cells. Methods: A lung cancer cell line was treated with Gundelia tournefortii extract. The metabolic content of the extract that plays key roles in anticancer was detected by high-performance liquid chromatography. Anticancer properties were further detected by a flow cytometer apoptosis assay, and signaling pathways were determined by a PCR array through hub gene expression alteration. Gene enrichment analysis and network pharmacology correlated metabolites and pathways that were involved in anticancer effects. Results: The metabolite content of G. tournefortii was analyzed, and gallic acid, clorogenic acid, hydroxybenzoic acid, caffeic acid, epicatechin, p-coumaric acid, salicylic acid, apigenin 7 glucoside, and cinnamic acid were detected as key compounds. Lung cancer cell line A549 was treated with the extract at increasing concentrations for 24, 48, and 72 h, and its effects on cell viability were determined by MTT analysis. A statistically significant difference was observed for IC₅₀ concentrations depending on incubation times. It was also observed that the G. tournefortii water extract significantly increased apoptosis in A549 cells in comparison with the control group. G. tournefortii extract’s effect on lung cancer cell line was measured using the signal pathway PCR array gene set. Gene enrichment analysis of the array expression data confirmed activation of apoptosis-related pathways, particularly the upregulation of BAX and downregulation of HSP90. Conclusions: These findings suggest that G. tournefortii metabolites provide promising selective anticancer drug candidates and potential drug templates to prevent side effects and resistance of current clinical drug treatments.

Background: Ulcerative colitis (UC) is characterized by chronic mucosal inflammation, oxidative stress, and disruption of intestinal metabolic homeostasis. Immunomodulatory nutrients such as arginine, glutamine, and β-hydroxy β-methylbutyrate (HMB) have shown potential benefits; however, their combined molecular effects on UC remain insufficiently defined. Objective: To investigate the individual and combined effects of arginine, glutamine, and HMB on inflammatory and metabolic gene expression, oxidative stress markers, and histopathological outcomes in a dextran sulfate sodium (DSS)-induced colitis model. Methods: Female Sprague Dawley rats were assigned to six groups: control, DSS, DSS + arginine, DSS + glutamine, DSS + HMB, and DSS + mixture. Colitis was induced using 3% DSS. Colon tissues were examined histologically, serum MDA, MPO, and GSH levels were quantified, and mRNA expression of IL6, IL10, COX2, NOS2, ARG2, CCR1, and ALDH4A1 was measured by RT-qPCR. Pathway enrichment analyses were performed to interpret cytokine and metabolic network regulation. Results: DSS induced severe mucosal injury, elevated MDA and MPO, reduced GSH, and significantly increased IL6, COX2, NOS2, ARG2, and CCR1 expression. Glutamine demonstrated the strongest anti-inflammatory and antioxidant effects by decreasing IL6 and COX2 and restoring GSH. Arginine primarily modulated nitric oxide–related pathways, whereas HMB increased ALDH4A1 expression and metabolic adaptation. The combination treatment produced more balanced modulation across inflammatory, chemokine, and metabolic pathways, consistent with enrichment results highlighting cytokine signaling and amino acid metabolism. Histopathological improvement was greatest in the mixture group. Conclusions: Arginine, glutamine, and HMB ameliorate DSS-induced colitis through coordinated regulation of cytokine networks, oxidative stress responses, and metabolic pathways. Their combined use yields broader and more harmonized therapeutic effects than individual administration, supporting their potential as targeted immunonutritional strategies for UC. Rather than targeting a single inflammatory mediator, this study was designed to test whether combined immunonutrient supplementation could promote coordinated regulation of cytokine signaling, oxidative stress responses, and metabolic adaptation, thereby facilitating mucosal repair in experimental colitis.