FENGYCIN/ MIR-34A-FENGYCIN COMPLEX: AN ALTERNATIVE THERAPEUTIC STRATEGY FOR HCT116 COLORECTAL CANCER CELL LINE
DOI:
https://doi.org/10.4238/1vsjb488Keywords:
Colorectal cancer, fengycin, miRNAs, miR-34a, HCT116 cell line, cell line transfection.Abstract
Background. The development of selective anticancer therapies remains a major challenge due to tumor heterogeneity and limited specificity of conventional treatments.
Aim: This study designd to evaluate the cytotoxic effect of fengycin/fengycin-miR-34a complex toward growth and proliferation of HCT116 colorectal cancer cell line.
Materials and methods: The interested protein in current study was extracted previously by the supplying company, MTT assay was used to evaluate the effects of fengycin/miR-34a-fengycin complex on cancerous HCT116 and Homo sapiens gingival fibroblast (HGF) cell line at variant dilutions (20, 30, and 40 μg /ml), RT-qPCR was depended to detect focused gene expression of K-ras, PIK3CA, TP53, and caspase-3 genes in both cell lines.
Results: Fengycin exhibited a dose-dependent increase in apoptosis in HCT116 colorectal cancer cells (5%, 27.6%, and 60% at 20, 30, and 40 μg/mL, respectively), with minimal effects on normal HGF cells (3%, 1%, and 4%; P=0.001). Transfection with miR-34a alone reduced HCT116 cell viability to 39.7%, while maintaining high viability in HGF cells (117%). Notably, the miR-34a–fengycin biocomplex (30 μg/mL protein / 2.5 nM miRNA) demonstrated the highest apoptotic rate in HCT116 cells (71.6%) compared to only 9.6% in HGF cells (P= 0.01). At the molecular level, this treatment significantly upregulated TP53 and caspase-3 expression (36.7- and 47.5-fold, respectively), with minimal changes in KRAS (1.1-fold) and slight elevation in PIK3CA (1.7-fold). In contrast, HGF cells showed marked upregulation of survival-related PIK3CA (442.9-fold) and KRAS (28.6-fold), with limited apoptotic signaling.
Conclusion: The miR-34a–fengycin biocomplex exerts potent and selective anticancer activity by enhancing apoptosis in cancer cells while preserving normal cell viability. This dual-action strategy highlights its potential as a promising targeted therapeutic approach for colorectal cancer.
Downloads
Published
Issue
Section
License

This work is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License.

