Antitumor Effects of Chrysophanol in Malignant Optic Nerve Meningioma Cell Lines are Mediated via Caspase Activation, Induction of Mitochondrial Mediated Apoptosis, Mitochondrial Membrane Depolarization and Targeting the Mitogen-Activated Protein Kinase Signaling Pathway

Zeng, Changhong; Guo, Bo; Chen, Jun; He, Weimin

doi:10.1159/000499336

Cited by 11 publications

(7 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has reported that chrysophanol has an anti-tumor role in the cell proliferation of lung cancer via mediating ROS/HIF-1a/VEGF signaling cascade [ 19 ]; additionally, it also suppresses cell growth, migration, and reactive oxygen species generation in oral cancer cell lines [ 20 ]. Moreover, it induces apoptosis of malignant optic nerve meningioma cells via inducing the caspase activation and targeting the MAPKs signaling cascade [ 21 ]. Similarly, our results in a menangioma cell type suggest that chrysophanol suppresses the proliferation of tumor cells while promoting their apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Chrysophanol inhibits the osteoglycin/mTOR and activats NF2 signaling pathways to reduce viability and proliferation of malignant meningioma cells

Jia-peng

2021

Bioengineered

View full text Add to dashboard Cite

Chrysophanol shows promising antitumor activity, but how it may work against malignant meningioma is poorly understood. In addition, osteoglycin (OGN) may help mediate the antitumor effects of chrysophanol; thus, this study investigated the potential antitumor mechanism of chrysophanol in malignant meningioma cultures. Meningioma cell line HBL-52 were incubated with varying doses of chrysophanol (0–90 μM) for different time points, and osteoglycin (OGN) was overexpressed or inhibited in some cell cultures to assess its roles. Cell viability was quantified using the CCK8 assay and colony formation assays, while effects on cell cycle distribution and apoptotic rates were examined by flow cytometry and enzyme-linked immunosorbent assays (ELISA) to detect histone DNA levels. Caspase-3 and −9 activities were detected by related commercial kits. Protein expression was assessed using Western blotting. Chrysophanol significantly reduced HBL-52 cell viability, based on reduced colony formation, and proliferation, based on low levels of bromodeoxyuridine incorporation. Annexin V/propidium iodide staining revealed a 30% increase in apoptotic cells at 90 μM chrysophanol (33.7% vs 3.3% in control cultures). Chrysophanol treatment greatly decreased the Bcl-2/Bax expression ratio and increased the expressions of cleaved caspase-3 and −9, and the activities of caspase-3 and −9. Chrysophanol blocked cells in G1 phase and inhibited the OGN/mTOR signaling cascade, but activated neurofibromatosis 2 (NF2) cascade. OGN overexpression activated mTOR, down-regulated NF2, and partially reversed growth inhibition by chrysophanol. Chrysophanol may be useful as a treatment against malignant meningioma by inhibiting OGN/mTOR signaling and activating NF2 signaling.

show abstract

Section: Discussionmentioning

confidence: 99%

Chrysophanol inhibits the osteoglycin/mTOR and activats NF2 signaling pathways to reduce viability and proliferation of malignant meningioma cells

Jia-peng

2021

Bioengineered

View full text Add to dashboard Cite

show abstract

“…Apoptosis was detected via concurrent staining with annexin V-CF647 and 7-aminoactinomycin D (7-AAD) using a commercial kit (FCCH100108, FlowCellect Õ annexin V red kit; Sigma-Aldrich). 18 ENCCs were aliquoted as 1 Â 10 6 cells/100 mL into FACS tubes. The cells were washed twice, centrifuged, and pelleted.…”

Section: Flow Cytometric Analysis Of Cell Cycle and Apoptosis Of Enccsmentioning

confidence: 99%

“…The detection of phosphatidylserine using fluorochrome-tagged anticoagulant protein annexin V enabled precise estimation of apoptotic incidence. 18 Early apoptotic cells bind annexin V but exclude 7-AAD (annexin V þ 7-AAD À ). 18 In this study, compared to that in the controls (6.62 AE 3.78% vs 6.69 AE 3.54%, P > .05), PTU did not change the Figure 3.…”

Section: Ptu Reduced the Mitotic Activity Of Enccsmentioning

confidence: 99%

See 1 more Smart Citation

Thyroid Hormone in the Pathogenesis of Congenital Intestinal Dysganglionosis

et al. 2020

View full text Add to dashboard Cite

Introduction The objective of this study is to investigate the role of thyroid hormone (TH) in the pathogenesis of intestinal dysganglionosis (ID). Methods A zebrafish model of congenital hypothyroidism (CH) was created by exposing the larvae to the 6-propyl-2-thiouracil (PTU). The enteric neurons were labeled with anti-HuC/D antibodies. The number of enteric neurons was counted. The larval intestine was dissociated and stained with anti-p75 and anti-α4 integrin antibodies. Mitosis and apoptosis of the p75+ α4 integrin+ enteric neural crest cells (ENCCs) were studied using flow cytometry. Intestinal motility was studied by analyzing the transit of fluorescent tracers. Results PTU (25 mg/L) significantly reduced TH production at 6- and 9-days post fertilization without changing the body length, body weight, and intestinal length of the larvae. Furthermore, PTU inhibited mitosis of ENCCs and reduced the number of enteric neurons throughout the larval zebrafish intestine. Importantly, PTU inhibited intestinal transit of fluorescent tracers. Finally, thyroxine supplementation restored ENCC mitosis, increased the number of enteric neurons, and recovered intestinal motility in the PTU-treated larvae. Conclusions PTU inhibited TH production, reduced the number of enteric neurons, impaired intestinal motility, and impeded ENCC mitosis in zebrafish, suggesting a possible role of CH in the pathogenesis of ID.

show abstract

“…Over the years, the pharmacological properties of chrysophanol have been researched; for example, resistant effects relative to inflammatory diseases, diabetes, bacterial, oxidation, ulcer, and cancer have been confirmed [ 31 , 32 ]. In addition, chrysophanol has shown potent anti-cancer effects on some cancers, such as liver, colon, and ovarian cancers [ 33 , 34 , 35 , 36 , 37 , 38 , 39 ].…”

Section: Introductionmentioning

confidence: 99%

Chrysophanol-Induced Autophagy Disrupts Apoptosis via the PI3K/Akt/mTOR Pathway in Oral Squamous Cell Carcinoma Cells

Park

et al. 2022

Medicina

View full text Add to dashboard Cite

Background and Objectives: Natural products are necessary sources for drug discovery and have contributed to cancer chemotherapy over the past few decades. Furthermore, substances derived from plants have fewer side effects. Chrysophanol is an anthraquinone derivative that is isolated from rhubarb. Although the anticancer effect of chrysophanol on several cancer cells has been reported, studies on the antitumor effect of chrysophanol on oral squamous-cell carcinoma (OSCC) cells have yet to be elucidated. Therefore, in this study, we investigated the anticancer effect of chrysophanol on OSCC cells (CAL-27 and Ca9-22) via apoptosis and autophagy, among the cell death pathways. Results: It was found that chrysophanol inhibited the growth and viability of CAL-27 and Ca9-22 and induced apoptosis through the intrinsic pathway. It was also found that chrysophanol activates autophagy-related factors (ATG5, beclin-1, and P62/SQSTM1) and LC3B conversion. That is, chrysophanol activated both apoptosis and autophagy. Here, we focused on the roles of chrysophanol-induced apoptosis and the autophagy pathway. When the autophagy inhibitor 3-MA and PI3K/Akt inhibitor were used to inhibit the autophagy induced by chrysophanol, it was confirmed that the rate of apoptosis significantly increased. Therefore, we confirmed that chrysophanol induces apoptosis and autophagy at the same time, and the induced autophagy plays a role in interfering with apoptosis processes. Conclusions: Therefore, the potential of chrysophanol as an excellent anticancer agent in OSCC was confirmed via this study. Furthermore, the combined treatment of drugs that can inhibit chrysophanol-induced autophagy is expected to have a tremendous synergistic effect in overcoming oral cancer.

show abstract

Antitumor Effects of Chrysophanol in Malignant Optic Nerve Meningioma Cell Lines are Mediated via Caspase Activation, Induction of Mitochondrial Mediated Apoptosis, Mitochondrial Membrane Depolarization and Targeting the Mitogen-Activated Protein Kinase Signaling Pathway

Cited by 11 publications

References 14 publications

Chrysophanol inhibits the osteoglycin/mTOR and activats NF2 signaling pathways to reduce viability and proliferation of malignant meningioma cells

Chrysophanol inhibits the osteoglycin/mTOR and activats NF2 signaling pathways to reduce viability and proliferation of malignant meningioma cells

Thyroid Hormone in the Pathogenesis of Congenital Intestinal Dysganglionosis

Chrysophanol-Induced Autophagy Disrupts Apoptosis via the PI3K/Akt/mTOR Pathway in Oral Squamous Cell Carcinoma Cells

Contact Info

Product

Resources

About