Magnolol Induces Oxidative Stress-Mediated Apoptosis in SKOV3 Cells by Targeting NF-Κb/TNF-Α/COX-2 And Cyclin D1/C-Myc/Survivin Pathways

Aggressive and recurring gynaecological malignancies are associated with a poor prognosis and ineffective treatment. Patients with ovarian cancer (OC) are frequently detected at an advanced stage, when medication resistance, angiogenesis, recurrence, and metastases all have an impact on survival. Ovarian cancer (OC) remains the deadliest gynaecologic tumor worldwide. Magnolol (ML), a natural bioactive neolignan, exhibits favourable pharmacological safety and potent anticancer activity. Recently, it has been reported that MAG exerts anticancer effects by inhibiting numerous cancer cell lineages. Thus, we explore the anti-tumor efficiency of MAG on human ovarian cancer (SKOV3) cells and its modulation of Janus kinase 2/signal transducers and activators of transcription 3/extracellular signal-regulated kinase (JAK2/STAT3/ERK) networks. The activity of MAG on SKOV3 cell viability, reactive oxygen species (ROS) generation, apoptotic markers, cytokines, apoptosis, and JAK2/STAT3/ERK networks was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test, dichlorodihydrofluorescein diacetate (DCFH-DA), 4',6-real-time polymerase chain reaction (RT-PCR) analysis. Our results exposed that MAG could reduce SKOV3 cell viability in a dose-dependent way, and 20mg was selected as the IC50 value for further mechanistic studies. Our findings established that MAG 20mg inhibited SKOV3 cell viability through enhanced intracellular ROS generation, and stimulated apoptosis compared to control. Likewise, ML moderated inflammatory cytokines, induced apoptotic markers, and instigated intracellular cell death pathways. Here, we proved that ML attenuates SKOV3 cell proliferation by ROS-facilitated apoptosis via suppression of the JAK2/STAT3/ERK pathways. Hence, ML may serve as a promising natural anticancer agent for OC management.