<p>Polyphyllin VI Induces Apoptosis and Autophagy via Reactive Oxygen Species Mediated JNK and P38 Activation in Glioma</p>

Abstract

Background: Polyphyllin VI (PPVI), a bioactive component derived from a traditional Chinese herb Paris polyphylla, exhibits potential antitumor activity against hepatocellular carcinoma, as well as breast and lung cancers. However, its effect on glioma remains unknown. Methods: Five glioma cell lines (U251, U343, LN229, U87 and HEB) and an animal model were employed in the study. Anti-proliferation effects of PPVI were first determined using CCK-8 cell proliferation and clone formation assays, then reactive oxygen species (ROS), cell cycle progression and apoptosis effects measured by flow cytometry. The effect of PPVI on protein expression was quantified by Western blot analysis. Results: Data showed that PPVI inhibited the proliferation of glioma cell lines by modulating the G2/M phase. Additionally, incubation of cells with PPVI promoted apoptosis, autophagy, increased accumulation of ROS and activated ROS-modulated JNK and p38 pathways. On the other hand, N-acetyl cysteine, a ROS inhibitor, attenuated PPVItriggered effects. Furthermore, JNK and p38 inhibitors ameliorated PPVI-triggered autophagy and apoptosis in glioma cells. In vivo assays showed that PPVI inhibited tumor growth of U87 cell line in nude mice. Conclusion: Overall, these data suggested that PPVI might be an effective therapeutic agent for glioma.

High Adenosine Extracellular Levels Induce Glioblastoma Aggressive Traits Modulating the Mesenchymal Stromal Cell Secretome

“…The effects of a wide range of ADO concentrations (from 10 nM to 100 µM) on U343MG proliferation and viability were evaluated after 24 or 48 h of cell treatment. The U343MG human glioblastoma cell line has been widely used to investigate the pathophysiological mechanisms of glioblastoma [ 45 , 46 ]; herein, we selected this cell line as a representative model to investigate the effects of ADO in the tumor microenvironment. The obtained results show extracellular ADO did not significantly increase cell proliferation after 24 or 48 h of treatment, even if a slight increase could be appreciated at the highest ADO concentrations at 48 h ( Figure 1 A,B).…”

<p>Genetic and Clinical Characterization of HOXB2 in Glioma</p>

“…The expression of proteins was detected using Western blot as previously described. 15 The primary antibodies used in the study were HOXB2 (ab136856) and MMP-2 (ab2462)(abcam, USA). β-actin (A8418) (Sigma, USA) was used as an internal control.…”

“…The invasion assay was performed using the transwell system (24wells, 8μm pore size with polycarbonate membrane, Corning Costar) as previously described. 15…”

“…Invasive growth has been recognized as a critical feature of glioma and plays a vital role in promoting tumorigenesis and development. 15,28 It is a complex biological process with multifactor and multicell involvement, including ECM degradation, epithelial-mesenchymal transition, and neovascularization. 29,30 ECM components are large molecules that are synthesized by cells, secreted to the outside of the cells, and become distributed on the surface of the cells or between cells.…”

Neferine induces apoptosis by modulating the ROS‑mediated JNK pathway in esophageal squamous cell carcinoma

“…Apoptosis refers to the active and orderly death of cells that maintains homeostasis of the internal environment under physiological or pathological conditions ( 17 , 18 ). Exposure of cells to internal pro-apoptotic factors, such as activators of oncogenes, agents that cause DNA damage, cell hypoxia, and deficiency of cell growth factors, has been revealed to activate apoptosis of mitochondrial cells ( 19 ).…”