title: Inhibitory effects of hyperoside on lung cancer by inducing apoptosis and suppressing inflammatory response via caspase-3 and NF-κB signaling pathway.
abstract: Lung cancer is one of the most common malignancies in the world and the most threatening cancer to human health. Effective therapies based on non-cytotoxic induction in cell inflammation- and apoptosis-responsive pathways are thought to represent a novel advance in treating lung cancer. However, many studies are still required for effective pharmaceutical to induce cancer cell death. Hyperoside (Hyp) is the chief component of some Chinese herbs with anticancer effect. Here, we investigated the role of hyperoside on the lung cancer cell migration, invasion, inflammation and apoptosis in A549 cells in vitro and xenografts of nude mice in vivo. A549 cells were injected in nude mice for establishing tumors. Our results showed that hyperoside suppressed the proliferation, migration and invasion. Additionally, apoptosis was induced by hyperoside via Bcl-2/Bax-regulated Caspase3 activation, suggesting that hyperoside might inhibit lung cancer progression through apoptotic induction. And also, hyperoside could prevent progression and development of lung cancer through inactivating NF-κB signaling pathway. Subsequently, inflammatory cytokines, including TNF-α, IL-6, IL-1β and IL-18, were down-regulated significantly. And animal experiments also illustrated that the tumor volume and weight were reduced after hyperoside administration, which was also through apoptosis induction and prevention of inflammation response by Caspase3 activation and NF-κB inactivation. To our knowledge, it was the first time to evaluate the effects of hyperoside on preventing progression and development of lung cancer in vivo and in vitro to assess the possible therapies of hyperoside as a future approach for preventing lung cancer progression and development.
authors.affiliation: Department of TCM, Taizhou First People's Hospital, Taizhou, Zhejiang 318020, China. Electronic address: lvping318020@163.com.
authors.forename: Ping
authors.initials: P
authors.lastname: Lü
mesh_terms: D000072283:A549 Cells; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000378:metabolism*; D002465:Cell Movement / Q000187:drug effects; D048430:Cell Shape / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D016207:Cytokines / Q000378:metabolism; D018450:Disease Progression; D006801:Humans; D007249:Inflammation / Q000473:pathology*; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000473:pathology*; D016328:NF-kappa B / Q000378:metabolism*; D009361:Neoplasm Invasiveness; D009569:Nitric Oxide / Q000096:biosynthesis; D011794:Quercetin / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D015398:Signal Transduction / Q000187:drug effects*
chemical_list: D016207:Cytokines; D016328:NF-kappa B; D009569:Nitric Oxide; C021304:hyperoside; D011794:Quercetin; D053148:Caspase 3
keywords: Apoptosis; Hyperoside; Inflammation response; Lung cancer