Macranthoside B Enhances Paclitaxel-induced Human Cervical Cancer Cell Apoptosis Through ROS-JNK Pathway

Abstract

Background/aim: This study aims to elucidate whether Macranthoside B (MB) intensifies paclitaxel (PTX)-induced apoptosis in human cervical adenocarcinoma HeLa cells as well as the underlying mechanisms.

Materials and methods: The MTT assay was used to test the HeLa cell viability after MB and PTX co-treatment, and colony formation assay was utilized to evaluate cell proliferation. Reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were analyzed by flow cytometry. Western blotting analysis was used to quantify the protein expression levels of MAPKs signaling pathway and apoptotic markers. ROS scavenger NAC and JNK specific inhibitor JNK-IN-8 were utilized to study the effects of ROS and JNK on HeLa cell apoptosis, respectively.

Results: Compared to MB or PTX sole treatment, MB-PTX co-incubation significantly inhibited HeLa cell proliferation, increased ROS overgeneration, and decreased MMP, leading to apoptosis. ROS scavenger and JNK inhibitor reverse MB-PTX-induced HeLa cell apoptosis by decreasing the activation of JNK pathway.

Conclusion: MB increases PTX-mediated HeLa cell apoptosis by overgeneration of ROS and activating MAPKs/JNK pathway.

Keywords: Macranthoside B; ROS/JNK; apoptosis; cervical cancer; paclitaxel; reactive oxygen species.