Ức chế tăng sinh tế bào và khả năng tạo cụm trên dòng ung thư đại trực tràng chuyển nạp hyper-IL-6 của protein tái tổ hợp sgp130Fc

Colorectal cancer (UTĐTT) remains a formidable global health challenge, characterized by high incidence and mortality rates despite advancements in conventional therapies. A critical aspect of its pathogenesis involves the complex interplay of inflammatory cytokines, notably Interleukin-6 (IL-6), which has been identified as a key driver of oncogenesis through pathways like JAK/STAT3 signaling. This signaling cascade not only promotes cell proliferation and angiogenesis but also fosters an immunosuppressive tumor microenvironment, contributing to disease progression and poor patient outcomes. Consequently, there is an urgent need for novel targeted molecular therapies. This study investigates the anti-cancer potential of recombinant sgp130Fc protein, a soluble gp130 receptor analogue, to specifically inhibit IL-6-mediated signaling in vitro and explore its promise as a new therapeutic agent against IL-6-enhanced colorectal cancer.

Researchers in oncology, molecular biology, immunology, and pharmacology; clinicians specializing in gastroenterology or oncology; and biotechnology professionals involved in cancer drug development.

This study explored the anti-cancer efficacy of recombinant sgp130Fc protein on human colorectal cancer (UTĐTT) cell lines, specifically HT29 hyper-IL-6 and HCT116 hyper-IL-6, which are genetically engineered to overexpress IL-6. The research focused on assessing the protein's ability to inhibit cell proliferation and colony-forming capacity using conditioned medium derived from HEK cells transfected with sgp130FcH. The methodology involved in vitro experiments, utilizing WST-1 assays to evaluate cell viability and Crystal Violet assays to quantify colony formation after treatment with the sgp130FcH conditioned medium compared to control HEK WT medium.

Results from WST-1 assays indicated a tendency for sgp130FcH conditioned medium to reduce cell viability in both HT29 and HCT116 hyper-IL-6 cell lines; however, this reduction was not statistically significant (p > 0.05). In contrast, Crystal Violet assays revealed a significant inhibition of colony formation, particularly potent in the HCT116 hyper-IL-6 line (p < 0.001). This suggests that while recombinant sgp130Fc protein may not acutely impact cell viability, it exerts a substantial inhibitory effect on the long-term growth and self-renewal capabilities of IL-6-enhanced colorectal cancer cells.

The findings underscore the potential of recombinant sgp130Fc protein as a targeted molecular therapy, especially for colorectal cancer cases characterized by dysregulated IL-6 signaling. By effectively inhibiting the colony-forming ability of these aggressive cancer cells in vitro, sgp130Fc could represent a promising new strategy to impede tumor progression and metastasis. Further in vivo investigations are crucial to validate these encouraging preclinical observations and pave the way for its clinical application.