Loading
Life sciences · Journal article
Journal of Herbmed Pharmacology · October 1, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Introduction: Breast cancer therapy often faces challenges with drug resistance and severe side effects, highlighting the urgent need for novel therapeutic agents. Trigonella foenum-graecum (TFG) contains steroid sapogenins with potential as anti-cancer agents. This study assessed the methanolic extract of TFG (METFG) against eight breast cancer cell lines. The novelty lies in uncovering p53-independent mechanisms and demonstrating its capacity to overcome initial therapeutic resistance by simultaneously blocking PI3K/AKT/mTOR survival pathways. Methods: TFG seeds were extracted using methanol, and the chemical components were analyzed via GC-MS. Cytotoxicity across eight breast cancer cell lines was evaluated using MTT assays across 24 and 48 hours. Furthermore, apoptosis, cell cycle progression, and the phosphorylation of DNA damage and PI3K/AKT/mTOR marker proteins were analyzed using flow cytometry and Western blot. Results: METFG demonstrated significant time-dependent cytotoxicity, reducing the IC₅₀ in MCF7 -/-p53 cells from 172.5±2.4 µg/mL at 24 hours to 134.3±7.2 µg/mL at 48 hours. The extract successfully induced apoptosis and triggered a cell-cycle phase shift, increasing the percentage of G2/M-phase cells to 29% in MDA-MB cell lines. Additionally, METFG significantly reduced phosphorylation of CHK1, CHK2, AKT, and mTOR, suggesting a potential inhibition of the DNA damage response and cell survival signaling. Conclusion: The endemic Karo METFG exhibits significant cytotoxic activity by inducing apoptosis, promoting cell cycle arrest, and suppressing DDR and PI3K/AKT/mTOR pathways. Future investigations must assess its selective toxicity against normal mammary epithelial cells to establish its safety.