ovatodiolide has been researched along with Glioblastoma* in 2 studies
2 other study(ies) available for ovatodiolide and Glioblastoma
| Article | Year |
|---|---|
Targeting FGL2, a molecular drug target for glioblastoma, with natural compounds through virtual screening method.
Topics: Antineoplastic Agents; Apoptosis; Betacyanins; Cell Proliferation; Computer Simulation; Diterpenes; Drug Screening Assays, Antitumor; Fibrinogen; Gene Expression Regulation; Glioblastoma; Hesperidin; Humans; Molecular Targeted Therapy; Protein Binding | 2021 |
Ovatodiolide inhibits the oncogenicity and cancer stem cell-like phenotype of glioblastoma cells, as well as potentiate the anticancer effect of temozolomide.
Ovatodiolide (Ova), a major bioactive diterpenoid isolate of Anisomeles indica has drawn considerable attention lately as an effective anticancer agent with several published works demonstrating its tumor-inhibitory activity in various cancer types.. In this study, we examined the modulatory effect of Ova on the oncogenicity, proliferation, and cancer stem cell-like traits of glioblastoma (GBM) cells, as well as investigated the underlying molecular mechanism for the anticancer activity of Ova in GBM cell lines, U-87MG and GBM8401.. The antiproliferative, apoptotic, and stemness-attenuating effects of Ova were evaluated using the sulforhodamine B (SRB) colorimetric assay, western blot and fluorescent immunocytochemistry. Cell apoptosis was analyzed based on variation in the expression levels of Bcl-2 family of regulator proteins Bax, Bak, Bcl-2 and Bcl-xL.. Ova induced the apoptosis of the U-87MG and GBM8401 cells, as well as effectively inhibited the proliferation and motility of the GBM cell lines in a dose- and time-dependent manner. Ova-induced apoptosis correlated with increased Bax/Bcl-2 ratio, while inhibition of tumor cell migration and colony formation was associated with reduced Slug, Vimentin, NCadherin and β-catenin protein expression and increased E-Cadherin. In addition, exposure to Ova inhibited tumorsphere formation, elicited downregulation of CD44, CD133, Sox2, and Oct4, as well as correlated with dysregulation of the JAK2-STAT3 signaling pathway. Furthermore, we showed for the first time to the best of our knowledge that Ova potentiate the chemotherapeutic effect of Temozolomide.. Taken together, our findings demonstrate the anticancer potential of Ova in GBM and its efficacy in the treatment of GBM as monotherapy and in combination with Temozolomide. Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; beta Catenin; Cell Line, Tumor; Diterpenes; Down-Regulation; Glioblastoma; Humans; Janus Kinase 2; Neoplastic Stem Cells; Proto-Oncogene Proteins c-bcl-2; Signal Transduction; SOXB1 Transcription Factors; STAT3 Transcription Factor; Temozolomide | 2019 |