Anticancer effects of Commiphora myrrha extract on colorectal cancer through regulation of metastasis, cell cycle progression, and apoptosis in vitro and in vivo.

Commiphora myrrha exhibits multiple pharmacological properties, including antioxidant, anti-inflammatory, antimicrobial, antidiabetic, and anticancer activities. Although the cytotoxic effects of C. myrrha have been observed in various cancer cell lines, the molecular mechanisms underlying its therapeutic potential against colorectal cancer (CRC) remain largely uncharacterized. In this study, we investigated the anticancer effects of C. myrrha extract (CMy) on CRC using in vitro and in vivo models. The anticancer properties of CMy were evaluated through MTT assay, colony formation, wound healing assay, invasion assay, cell cycle analysis, and terminal deoxynucleotidyl transferase dUTP nick-end labeling staining. Western blotting was performed to detect the expression of proteins associated with cell cycle progression and apoptosis. The in vivo antitumor efficacy of CMy was investigated in a CRC-bearing BALB/c mouse model. This study revealed that CMy significantly decreased the viability, colony-forming ability, and the migratory and invasive capacities of CRC cells. Mechanistically, CMy induced G0/G1 phase cell cycle arrest through the downregulation of cyclin-dependent kinase 4 and cyclin D1 and promoted apoptosis by upregulating pro-apoptotic markers, including Bcl-2-associated X, caspase-9, and caspase-3. Furthermore, CMy exhibited a synergistic cytotoxic effect when combined with 5-fluorouracil, thereby enhancing its inhibitory activity against CRC cells. In vivo, CMy treatment effectively suppressed tumor progression and prolonged the survival of tumor-bearing mice at well-tolerated doses. Collectively, these findings indicate that CMy is a promising source of cytotoxic phytochemicals with significant anti-CRC activity, supporting its potential application as a therapeutic agent for CRC.