“…As an active process of cell death, apoptosis can be triggered through mitochondrial apoptosis pathway [27,28]. What's more, it has been reported that chrysophanol has anticancer activities, including induction of cell apoptosis by mitochondrial apoptosis pathway [15,25]. Thereby, we presumed that chrysophanol might play a part in glioma cells via mitochondrial pathway.…”
Section: Discussionmentioning
confidence: 85%
“…Glioma is a kind of brain tumor in human central nervous system with high mortality and relapse rates [3,30]. And more evidence has been accumulated to validate the repressive function of chrysophanol on cell development [15,[21][22][23][24][25]. For example, it has been reported that chrysophanol inhibits the osteoglycin/mTOR and activates NF2 signaling pathways to reduce viability and proliferation of malignant meningioma cells [31].…”
Section: Discussionmentioning
confidence: 99%
“…In addition, chrysophanol represses cell proliferation of colon cancer via epidermal growth factor receptor (EGFR)/ mammalian target of rapamycin (mTOR) signaling proteins such as extracellular signal-regulated kinase 1/2 (ERK1/2), P70S6K and AKT [22]. And the similar suppressive function of chrysophanol has been presented on breast, lung and ovarian cancers [15,[23][24][25]. However, the effect and mechanism of chrysophanol on glioma remain unclear.…”
Section: Introductionmentioning
confidence: 99%
“…It is reported that intrinsic pathway, namely mitochondrial pathway, is one of the important signaling cascades controlling cell apoptosis [28,29]. Previous studies have revealed that chrysophanol induces cell apoptosis by mitochondrion-related pathway in lung and ovarian cancer [15,25]. Therefore, we attempted to explore whether chrysophanol exerts an effect on glioma through mitochondrial apoptosis pathway.…”
Glioma is a common intracranial tumor originated from neuroglia cell. Chrysophanol is an anthraquinone derivative proved to exert anticancer effects in various cancers. This paper investigated the effect and mechanism of chrysophanol in glioma. Glioma cell lines U251 and SHG-44 were adopted in the experiments. The cells were treated with chrysophanol at different concentrations (0, 10, 20 50, 100 and 200 μM) for 48 h in the study, and then processed with MitoTempo. Mitochondria and cytosol were isolated to investigate the role of mitochondria during chrysophanol functioning on glioma cells. Cell viability was detected through 3-(4,5-Dimethyl-2-Thiazolyl)-2,5-Diphenyl Tetrazolium Bromide (MTT) assay, and cell apoptosis, cell cycle as well as relative reactive oxygen species (ROS) were assessed by flow cytometry. Expressions of Cytosol Cyt C, cleaved caspase-3, cleaved caspase-9, Cyclin D1 and Cyclin E were evaluated by western blot. In U251 and SHG-44 cells, with chrysophanol concentration rising, cell viability, expressions of Cyclin D1 and Cyclin E were decreased while cell apoptosis, levels of cleaved caspase-3, cleaved caspase-9 and Cytosol Cyt C as well as ROS accumulation were increased with cell cycle arrested in G1 phase. Besides, chrysophanol promoted ROS accumulation, cell apoptosis and transfer of Cyt C from mitochondria to cytosol in cells while MitoTempo partly reversed the effect of chrysophanol. Chrysophanol promoted cell apoptosis via activating mitochondrial apoptosis pathway in glioma.
“…As an active process of cell death, apoptosis can be triggered through mitochondrial apoptosis pathway [27,28]. What's more, it has been reported that chrysophanol has anticancer activities, including induction of cell apoptosis by mitochondrial apoptosis pathway [15,25]. Thereby, we presumed that chrysophanol might play a part in glioma cells via mitochondrial pathway.…”
Section: Discussionmentioning
confidence: 85%
“…Glioma is a kind of brain tumor in human central nervous system with high mortality and relapse rates [3,30]. And more evidence has been accumulated to validate the repressive function of chrysophanol on cell development [15,[21][22][23][24][25]. For example, it has been reported that chrysophanol inhibits the osteoglycin/mTOR and activates NF2 signaling pathways to reduce viability and proliferation of malignant meningioma cells [31].…”
Section: Discussionmentioning
confidence: 99%
“…In addition, chrysophanol represses cell proliferation of colon cancer via epidermal growth factor receptor (EGFR)/ mammalian target of rapamycin (mTOR) signaling proteins such as extracellular signal-regulated kinase 1/2 (ERK1/2), P70S6K and AKT [22]. And the similar suppressive function of chrysophanol has been presented on breast, lung and ovarian cancers [15,[23][24][25]. However, the effect and mechanism of chrysophanol on glioma remain unclear.…”
Section: Introductionmentioning
confidence: 99%
“…It is reported that intrinsic pathway, namely mitochondrial pathway, is one of the important signaling cascades controlling cell apoptosis [28,29]. Previous studies have revealed that chrysophanol induces cell apoptosis by mitochondrion-related pathway in lung and ovarian cancer [15,25]. Therefore, we attempted to explore whether chrysophanol exerts an effect on glioma through mitochondrial apoptosis pathway.…”
Glioma is a common intracranial tumor originated from neuroglia cell. Chrysophanol is an anthraquinone derivative proved to exert anticancer effects in various cancers. This paper investigated the effect and mechanism of chrysophanol in glioma. Glioma cell lines U251 and SHG-44 were adopted in the experiments. The cells were treated with chrysophanol at different concentrations (0, 10, 20 50, 100 and 200 μM) for 48 h in the study, and then processed with MitoTempo. Mitochondria and cytosol were isolated to investigate the role of mitochondria during chrysophanol functioning on glioma cells. Cell viability was detected through 3-(4,5-Dimethyl-2-Thiazolyl)-2,5-Diphenyl Tetrazolium Bromide (MTT) assay, and cell apoptosis, cell cycle as well as relative reactive oxygen species (ROS) were assessed by flow cytometry. Expressions of Cytosol Cyt C, cleaved caspase-3, cleaved caspase-9, Cyclin D1 and Cyclin E were evaluated by western blot. In U251 and SHG-44 cells, with chrysophanol concentration rising, cell viability, expressions of Cyclin D1 and Cyclin E were decreased while cell apoptosis, levels of cleaved caspase-3, cleaved caspase-9 and Cytosol Cyt C as well as ROS accumulation were increased with cell cycle arrested in G1 phase. Besides, chrysophanol promoted ROS accumulation, cell apoptosis and transfer of Cyt C from mitochondria to cytosol in cells while MitoTempo partly reversed the effect of chrysophanol. Chrysophanol promoted cell apoptosis via activating mitochondrial apoptosis pathway in glioma.
“…Under hypoxic conditions, HIF-1α is not hydroxylated, remains stable and accumulates. Subsequently, HIF-1α and hypoxia-inducible factor 1- beta (HIF-1β) combine to form HIF-1 in the cell nucleus, activating (through influence on DNA): angiogenesis, indirectly through VEGF, erythropoiesis and glycolysis enzymes [ [37] , [38] , [39] , [40] ]. Fig.…”
Section: Hypoxia-regulated Expression Of Glut In Glioblastomamentioning
Background
Fructose is a very common sugar found in natural foods, while current studies demonstrate that high fructose intake is significantly associated with increased risk of multiple cancers and more aggressive tumor behavior, but the relevant mechanisms are not fully understood.
Methods
Tumor-grafting experiments and in vitro angiogenesis assays were conducted to detect the effect of fructose and the conditioned medium of fructose-cultured tumor cells on biological function of vascular endothelial cells (VECs) and angiogenesis. 448 colorectal cancer specimens were utilized to analyze the relationship between Glut5 expression levels in VECs and tumor cells and microvascular density (MVD).
Results
We found that fructose can be metabolized by VECs and activate the Akt and Src signaling pathways, thereby enhancing the proliferation, migration, and tube-forming abilities of VECs and thereby promoting angiogenesis. Moreover, fructose can also improve the expression of vascular endothelial growth factor (VEGF) by upregulating the production of reactive oxygen species (ROS) in colorectal cancer cells, thus indirectly enhancing the biological function of VECs. Furthermore, this pro-angiogenic effect of fructose metabolism has also been well validated in clinical colorectal cancer tissues and mouse models. Fructose contributes to angiogenesis in mouse subcutaneous tumor grafts, and MVD is positively correlated with Glut5 expression levels of both endothelial cells and tumor cells of human colorectal cancer specimens.
Conclusions
These findings establish the direct role and mechanism by which fructose promotes tumor progression through increased angiogenesis, and provide reliable evidence for a better understanding of tumor metabolic reprogramming.
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