The tumor microenvironment, especially that of fibroblasts, strongly promotes colorectal cancer (CRC) progression. Progressive cancers usually accumulate high reactive oxygen species (ROS), leading to oxidative stress. The stress relates to the expression of thioredoxin reductase-1 (TrxR-1), which is an oxidative stress sensitivity molecule. This study aimed to investigate TrxR-1 expression as an indication of colon-fibroblast-inducing colorectal cancer progression and metastasis. We found that the high proliferative fibroblast-cultured media (FCM) contained pro-inflammatory cytokines that have a high ability to influence HCT116 and CRC cell progression, when compared with complete media (CM) as a control in terms of growth (CM = 100.00%, FCM = 165.96%), migration (CM = 32.22%, FCM = 83.07%), invasion (CM = 130 cells/field, FCM = 449 cells/field), and EMT transformation while decreasing E-cadherin expression (CM = 1.00, FCM = 0.69) and shape factor (CM = 0.94, FCM = 0.61). In addition, the overexpression of TrxR-1 is associated with cellular oxidant enchantment in FCM-treated cells. A dot plot analysis showed a strong relation between the EMT process and the overexpression of TrxR-1 in FCM-treated cells (CM = 13/100 cells, FCM = 45/100 cells). The cancer transplantation of the adult zebrafish model illustrated a significantly higher number of microtumors in FCM-treated cells (CM = 4.33 ± 1.51/HPF, FCM = 25.00 ± 13.18/HPF) disseminated in the intraperitoneal cavity with TrxR-1 positive cells. The overexpression of TrxR-1 indicated fibroblast-associated CRC progression in HCT116 cells and the zebrafish model. Therefore, TrxR-1 could be applied as a novel biomarker for colorectal cancer progression and prognostic evaluation.

Introduction: Green Curmin is a soluble curcumin extract product made in Thailand and reported to reduce gastric inflammation. Inflammatory cytokines including IL-1α, IL-6 and TNF-β play a crucial role in cancer cell migration, which is a major process towards poor prognosis. Objective: To investigate the effects of Green Curmin on colon cancer cell growth and migration, which involve the pro-inflammatory cytokines. Method: Curcuma longa, L. were extracted and named as Green Curmin. The cytotoxicity of the Green Curmin-treated HCT116-colon cancer cells was obtained by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry. The effect of the extract on cancer migration was investigated with wound healing assay. In addition, fibroblast-associated cancer migration was confirmed by using Transwell migration assay. Pro-inflammatory cytokines were also determined. Results: Green Curmin had cytotoxicity in the induced-cancer cell apoptosis at concentrations of 1 and 5 mg/ml. However, at concentrations of 0.05 and 0.1 mg/ml (non-toxicity dose), andreduced colon cancer migration and fibroblast associated-cancer migration. They also suppressed pro-inflammatory cytokines expression including IL-1α, IL-6 and TNF-β in colon cancer cells and IL-6 in fibroblast cells. Conclusion: Green Curmin suppressed pro-inflammatory cytokines and reduced fibroblast associated-cancer migration.

Porcine epidemic diarrhea virus (PEDV) continues to cause devastating economic losses in the swine industry. However, the lack of species-specific in vitro models and reliance on costly animal models hinders development of effective interventions. We established a high-fidelity platform using porcine induced pluripotent stem cells (piPSCs; line VSMUi001-C) via a 28-day stepwise differentiation protocol. Successful lineage commitment was validated by OCT4 downregulation and robust FOXA2/SOX17 expression at day 5. By day 28, the piPSC-derived intestinal epithelial cells (piPSC-IECs) exhibited organized LGR5+ niches, MUC2+ goblet cells, and Villin+ enterocytes, mirroring native tissue architecture. Barrier functionality was confirmed by the continuous distribution of the tight junction protein zonula occludens-1 (ZO-1). Our results demonstrate that piPSC-IECs are permissive to PEDV and support productive infection, encompassing the complete viral life cycle from entry to release of infectious progeny. Productive replication was confirmed by direct immunodetection of viral antigen within inoculated cells. Viral challenge induced characteristic cytopathic effects and a specific pro-inflammatory elevation of tumor necrosis factor-alpha (TNF-α). Notably, infection fragmented ZO-1, providing a mechanistic explanation for the leaky gut phenotype observed in vivo. This platform serves as a robust system for investigating viral kinetics and host–pathogen interactions with high species-specific relevance.