Work

Scutellarin regulates MAPK/ERK signalling in nasopharyngeal cancer via the apoptotic and ROS induced DNA damage

Year: 2026

Type: article

Abstract: • NPC - significant risk to public health in areas where it is endemic. • Scutellarin fights cancer by acting on a variety of signaling pathways. • NPC cells were exposed to scutellarin (20 and 30 μM/ml). • Proliferation and apoptosis were evaluated. • Inducing apoptosis via the signaling pathways. • Scutellarin may be effective conventional therapeutic drug. Nasopharyngeal carcinoma (NPC) occurs frequently, and NPC poses a significant risk to public health in areas where it is endemic. Better care is needed because NPC is associated with considerable morbidity and mortality. A natural anticancer substance called scutellarin fights cancer by acting on a variety of signalling pathways. Nevertheless, little is known about the underlying apoptotic and anti-proliferative actions of scutellarin. The current study aimed to determine the molecular effects of in vitro scutellarin on CNE1 human NPC cells through mechanisms such as cell proliferation, anti-inflammatory, and anti-apoptotic effects. NPC cells were exposed to scutellarin (20 and 30 μM/ml), and their proliferation and apoptosis were evaluated using the MTT assay, AO/EB, Rh-123, DCFH-DA, DAPI, and PI staining, cell adhesion, cell migration, and western blot analysis. We evaluated putative molecular pathways, MAPKs/NF-κB signaling, MMP, and intracellular ROS, cell proliferation regulatory proteins. By generating intracellular ROS, causing MMP loss and inducing apoptosis via the signalling pathways of TNF-α, COX-2, iNOS, and IL-6, pRB, cyclin-D1, CDK4/CDK6, and MAPKs/NF-κB, it has been found that scutellarin may reduce the proliferative, inflammatory, migratory, and invasive capacity of NPC cells. Our research supports the MAPKs/NF-κB pathway as a therapeutic target and suggests that it may play a key role in mediating the scutellarin actions against nasopharyngeal cancer malignancy. In summary, scutellarin may be an effective conventional therapeutic drug in preventing the progression of NPC.

Source: Translational Oncology

DOI: 10.1016/j.tranon.2025.102635