Effects of Hydatid Cyst Fluid on Inflammation and Epithelial-Mesenchymal Transition in Colorectal Adenocarcinoma (Caco-2) Cell Line
摘要
Anti-tumor immune responses and certain pathogens can exhibit various effects, including signals that reduce the risk of tumor formation or lead to cancer regression. Multiple studies have reported that infectious agents and the products of a wide range of host structures can modulate cancer development and growth positively or negatively and regulate the activation of immune responses. Numerous studies have reported that the parasite Echinococcus granulosus may have anti-cancer or carcinogenic effects on cancer cell proliferation in various cell cultures and animal models. The primary purpose of the study is to investigate the effect of animal-derived hydatid cyst fluid (HCF) at various concentrations (1/2, 1/3, 1/5) on the viability of human colorectal adenocarcinoma (Caco-2) and human colon epithelial (CoEpi) cell lines using the cell proliferation assay (XTT).
MethodsSubsequently, the study aims to investigate cytokine concentrations and gene expression profiles of inflammatory cytokines TNF-α and IL-4, as well as epithelial-mesenchymal transition (EMT) regulatory signaling proteins TGF- β1, vimentin and E-cadherin, using ELISA and RT-PCR methods, respectively.
ResultsFollowing the HCF application, EMT was consistently detected in the Caco-2 cell line compared to the CoEpi cell line in the 1/5 volume application group, as confirmed by ELISA, RT-PCR and cell proliferation assays. On the other hand, a linear relationship was observed between the levels of TGF-β1 and TNF-α, which regulate the pro-inflammatory signaling mechanism based on the cell micro-environment and the decrease in cell viability. As the HCF concentration volume decreased (1/5), an increase in cell viability was observed (P < 0.01), along with an increase in TGF-β1 and TNF-α levels. Otherwise, in Caco-2 cells, as the HCF application concentrations increased (1/2), significant decreases in TGF-β1 and TNF-α levels, as well as in cell viability, were observed (P < 0.01).
ConclusionsIn this context, the common antigen-receptor structure between E. granulosus and cancer may modulate the signals of the immune response it regulates, affecting immune system cells and contributing to the progression of tumor cells.