THERAPEUTIC POTENTIAL OF SELENOCYSTINE AND 5-FU IN TUMOR PROGRESSION VIA MODULATION OF THE JAK/STAT AND IMMUNE CHECKPOINT PATHWAYS
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Keywords
Breast cancer, MCF-7 cells, Selenocystine, 5-Fluorouracil, JAK/STAT signaling
Abstract
Breast cancer continues to pose a substantial worldwide health concern, requiring the investigation of innovative therapeutic approaches. This research examines the anticancer efficacy of Selenocystine and 5-Fluorouracil (5-FU) in human breast cancer MCF-7 cell lines. The MTT assay was utilised to evaluate cell viability after treatment with different concentrations (2–15 µM) of Selenocystine, 5-FU, and their combination. The findings indicated a dose-dependent decline in cell viability, with the combination therapy exhibiting the most significant cytotoxic impact, attaining an IC50 of 5.37 µM, in contrast to 7.02 µM for Selenocystine and 8.01 µM for 5-FU alone. Flow cytometry analysis revealed a substantial rise in the Sub-G1 and G0/G1 cell cycle populations, along with a notable decrease in the S and G2/M phases, indicating cell cycle arrest and the activation of apoptosis. Additionally, quantitative real-time PCR analysis demonstrated a significant downregulation of Janus Kinase/Signal Transducer and Activator of TranscriptionJ (AK/STAT) gene expression following treatment, with the combination therapy producing the most pronounced drop. The results indicate that Selenocystine augments the lethal effectiveness of 5-FU, offering a viable combinatorial approach for breast cancer therapy by facilitating apoptosis and inhibiting oncogenic signalling pathways. Subsequent research should concentrate on clarifying the fundamental molecular pathways and assessing in vivo efficacy to confirm the therapeutic potential of this combination.
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