Eriodictyol Inhibits Oral Cancer Proliferation and Activates ROS-mediated Apoptosis via the Attenuation of MAPK/STAT-3 Signaling Pathways
نویسندگان
1 Department of Clinical Laboratory, Xingtai People’s Hospital Xingtai, Hebei Prov-ince-054001, China
2 Department of Oral, Xingtai People’s Hospital Xingtai, Hebei Province-054001, China
3 Department of Clinical Laboratory, Xingtai People’s Hospital Xingtai, Hebei Prov-ince-054001, China
4 Department of Clinical Laboratory, Xingtai People’s Hospital Xingtai, Hebei Prov-ince-054001, China
doi
10.22034/ircmj.2025.446442.1047چکیده
Background and Objectives: Oral cancer (OC) remains a prominent cause of mortality worldwide. Eriodictyol (ERD) is a natural flavonoid that has been documented to exert antioxidant, anti-inflammatory, and anti-tumor activities. However, the precise role and the antitumor mechanism of ERD on OC are still uncertain. Methods: Hence, this study intended to explore the potential anticancer activity and underlying apoptotic mechanisms of ERD (30 and 40 µM/ml) in human oral squamous cell carcinoma (OSCC) SCC131 cells. The ERD activity on SCC131 cells cytotoxicity, intracellular ROS, apoptosis, MAPK/STAT-3 and P13K/AKT signaling pathways was assessed by MTT test, DCFH-DA, AO/EB, DAPI, PI, RT-PCR, and western blot analysis. Results: Our results uncovered that ERD could inhibit SCC131 cell viability, ROS accumulation, and enhanced apoptosis in a quantity dependent mode. ERD also alleviates the mRNA expression level of pin-1, STAT-3, p38, JNK, and p65 along with the protein level expression of the P13K/AKT signaling pathway as evidenced by western blot. Conclusion: Our data established that ERD attenuates SCC131 cell proliferation by ROS-mediated apoptosis through the inhibition of MAPK/STAT-3 and P13K/AKT signaling pathways suggesting that ERD is a potential natural remedy for OSCC.
