Molecular characterization of the anticancer properties associated with bee venom and its components in glioblastoma multiforme. (25th September 2021)

• Record Type: Journal Article
• Authors: Lebel, Andréa A.; Kisembo, Michée V.; Soucy, Marie-France N.; Hébert, Mathieu P.A.; Morin, Pier Jr; Boudreau, Luc H.
• Is Part Of: Chemico-biological interactions. Volume 347(2021)
• Publication Date: 2021-09-25
• Subjects: Brain tumor -- Glioma -- Cancer -- Apitoxin -- Apoptosis -- Non-coding RNAs; BV Bee venom -- BVPLA2 Phospholipase A2 from bee venom -- Mel Melittin; Biochemistry -- Periodicals; Toxicological chemistry -- Periodicals; Biochemistry -- Periodicals; Biologie moléculaire -- Périodiques; Biochimie -- Périodiques; Toxicologie biochimique -- Périodiques; 572
• DOI: 10.1016/j.cbi.2021.109622
• Languages: English
• ISSNs: 0009-2797

Abstract

Abstract: Glioblastoma multiforme (GBM) is a frequent form of malignant glioma. Strategic therapeutic approaches to treat this type of brain tumor currently involves a combination of surgery, radiotherapy and chemotherapy. Nevertheless, survival of GBM patients remains in the 12–15 months range following diagnosis. Development of novel therapeutic approaches for this malignancy is therefore of utmost importance. Interestingly, bee venom and its components have shown promising anti-cancer activities in various types of cancer even though information pertaining to GBMs have been limited. The current work was thus undertaken to better characterize the anti-cancer properties of bee venom and its components in Hs683, T98G and U373 human glioma cells. MTT-based cell viability assays revealed IC50 values of 7.12, 15.35 and 7.60 μg/mL for cell lines Hs683, T98G and U373 treated with bee venom, respectively. Furthermore, melittin treatment of these cell lines resulted in IC50 values of 7.77, 31.53 and 12.34 μg/mL, respectively. Cell viability assessment by flow cytometry analysis confirmed signs of late apoptosis and necrosis after only 1 h of treatment with either bee venom or melittin in all three cell lines. Immunoblotting-based quantification of apoptotic markers demonstrated increased expression of Bak and Bax, while Caspsase-3 levels were significantly lower when compared to control cells. Quantification by qRT-PCR showed increased expression levels of long non-coding RNAs RP11-838N2.4 and XIST in glioma cells treated with either bee venom or melittin. Overall, this study provides preliminary insight on molecular mechanisms via which bee venom and its main components can impact viability of glioma cells and warrants further investigation of its anticancer potential in gliomas. Highlights: Bee venom and Melittin induced a dose response in glioma cell lines. Melittin did not affect cell viability of immune blood cells at 5 μg/mL. Bee venom and Melittin caused modulations in various lncRNA in glioma cells. Early stages of apoptosis are induced after 1 h of Bee venom and Melittin treatments. Bee venom or Melittin with TMZ induced synergism effect at specific concentrations.