We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Ursolic Acid Suppresses Proliferation and Elicits Apoptosis of Laryngeal Carcinoma Cell HEp-2 through Activation of ROS Synthesis and Inhibition of Multiple Signaling Pathways
Summary
Researchers investigated the anticancer effects of ursolic acid on laryngeal squamous cell carcinoma HEp-2 cells, finding that it suppressed proliferation and induced apoptosis by stimulating reactive oxygen species (ROS) synthesis. The ROS increase was linked to activation of MAPK, PI3K/Akt, NF-κB, and STAT3 signaling pathways, positioning ursolic acid as a potential phytochemical therapeutic candidate for laryngeal carcinoma.
Abstract Laryngeal squamous cell carcinoma is one of the most common cancer-related causes of death worldwide. Thus, there is a constant need for improvement in drug development to promote treatment of this malignancy. In the present study, we identified a natural phytochemical, Ursolic acid, as a potent compound to counter laryngeal squamous cell carcinoma using HEp-2 cell line. Ursolic acid is capable of impeding proliferation and provoking apoptosis of HEp-2 cells. Interestingly, these anti-proliferative and proapoptotic effects is attributed to stimulation of ROS synthesis. In addition, we discovered that this UA-induced ROS stimulation is linked to the activation of MAPKs, PI3K/Akt, NF-κB and STAT3 signaling pathways. Our study characterized Ursolic acid as a potent anti-carcinoma drug with a multitargeting strategy, which enable it a novel and plausible treatment to laryngeal squamous cell carcinoma.
Sign in to start a discussion.
More Papers Like This
Morroniside Protects Human Granulosa Cells against H2O2-Induced Oxidative Damage by Regulating the Nrf2 and MAPK Signaling Pathways
Researchers found that morroniside protects human ovarian granulosa cells from oxidative damage by activating the Nrf2 antioxidant pathway and reducing apoptosis through regulation of p38 and JNK signaling pathways.
The Essential Oil from Conyza bonariensis (L.) Cronquist (Asteraceae) Exerts an In Vitro Antimelanoma Effect by Inducing Apoptosis and Modulating the MAPKs, NF-κB, and PKB/AKT Signaling Pathways
Researchers investigated the anticancer potential of an essential oil extracted from Conyza bonariensis against melanoma cells in laboratory experiments. They found that the oil's major compound interacted with key signaling pathways involved in cell survival and induced programmed cell death in melanoma cells. The study suggests this plant-derived compound may warrant further investigation as a potential source of anti-melanoma agents.
Ethanol Extract of Rosa rugosa Ameliorates Acetaminophen-Induced Liver Injury via Upregulating Sirt1 and Subsequent Potentiation of LKB1/AMPK/Nrf2 Cascade in Hepatocytes
Researchers prepared an ethanol extract from Rosa rugosa flower buds and found it significantly reduced liver damage caused by acetaminophen overdose in both cell and mouse models. The extract worked by activating the Sirt1 protein and boosting a protective signaling pathway that counters oxidative stress in liver cells. The study suggests Rosa rugosa extract may have potential as a natural intervention for drug-induced liver injury.
Hesperidin inhibits tobacco smoke‑induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway
Researchers found that hesperidin, a natural flavonoid compound, inhibits tobacco smoke-induced lung cell proliferation and epithelial-mesenchymal transition in mice by suppressing the p38 signaling pathway, suggesting a potential role in reducing lung cancer risk.
Integration of transcriptomics and metabolomics reveals the mechanism of Lycium barbarum polysaccharides inhibited MCF-7 cell proliferation
Researchers used transcriptomics and metabolomics to investigate how Lycium barbarum polysaccharides inhibit MCF-7 breast cancer cell proliferation, identifying the molecular mechanisms and signaling pathways responsible for the compound's anticancer activity at an optimal dose of 8 mg/mL.