Oridonin triggers G2/M cell cycle arrest, cellular apoptosis and autophagy in human gastric cancer cells
Purpose: Gastric carcinoma is the fourth principal cause of cancer-related deaths throughout the globe. There are inadequate clinical therapies for gastric cancer due to lack of operational drugs and ambiguity in molecular mechanisms. As such there is a persistent requirement for novel and effective anticancer drugs for gastric cancer. The main purpose of the current study was to investigate the antitumor effects of a plant diterpenoid, namely Oridonin, against SGC-7901 human gastric cancer cells along with examining its effects on cellular apoptosis, cell autophagy and cell cycle phase distribution.
Methods: WST-1 cell proliferation assay was used to evaluate cell viability of SGC-7901 human gastric cancer cells. Apoptosis was evaluated by using DAPI and comet assays using fluorescence microscopy. Autophagy was evaluated by transmission electron microscopy (TEM) and western blot method. Effects on cell cycle phase distribution were studied by flow cytometry.
Results: Oridonin molecule led to considerable and dose-dependent antiproliferative effects on SGC-7901 human gastric cancer cells exerting only mild cytotoxic effects in normal cells thus exhibiting selective toxicity. The number of gastric cancer cell colonies decreased significantly as oridonin dose increased. DAPI and comet assays revealed that oridonin induced powerful apoptotic effects in these cells, triggering significant DNA damage and both these effects exhibited dose-dependence. TEM indicated that oridonin induced autophagy in SGC-7901 cells by creating autophagosomes and autophagic vacuoles. Oridonin also targeted G2/M phase cell cycle in these gastric cancer cells along with targeting some key cell cycle related proteins including cyclin-B1, cyclin D1 and cyclin E.
Conclusion: In conclusion, the results show that oridonin showed strong anticancer effects in SGC-7901 human gastric cancer cells by triggering apoptosis and autophagy, and targeting cell cycle at G2/M phase.
Anticancer effects of α-mangostin in OVACAR-3 human ovarian carcinoma cells are mediated via involvement of reactive oxygen species, mitochondrial -mediated apoptosis, suppression of cell migration and invasion and m-TOR/PI3K/AKT signaling pathway
Purpose: α-mangostin belongs to xanthone class of natural products, showing a great biological and pharmacological potential. α-mangostin has shown remarkable anticancer potential against different cancer cell lines. Herein, α-mangostin was tested for its anticancer potential against human ovarian cancer cell line (OVACAR-3). Its effects on reactive oxygen species (ROS), mitochondrial-mediated apoptosis, cell migration and invasion and m-TOR/PI3K/AKT signaling pathway, was also determined.
Methods: MTT assay was performed to evaluate the rate of proliferation and clonogenic assay was used to assess the effects of α-mangostin on OVACAR-3 cell colonies. Phase contrast microscopy was implemented to evaluate cellular morphology. Acridine orange (AO) and ethidium bromine (EB) staining was used to check apoptosis along with western blotting. JC-1 and DCFH-DA staining assays were performed for the determination of mitochondrial membrane potential (MMP) and ROS, respectively. Cell migration and invasion analysis was performed with transwell chambers assay. The effect on m-TOR/PI3K/AKT signaling pathway was monitored by western blotting assay.
Results: α-mangostin had a tremendous inhibitory effect on cell proliferation rate in OVACAR-3 cells in a dose-dependent manner. The number of colonies was also observed to decline in a dose-dependent manner. Phase contrast microscopy showed significant morphological changes in OVACAR-3 cells after α-mangostin exposure. The antiproliferative effects were due to mitochondrial-mediated apoptosis. MMP was decreased by α-mangostin exposure and ROS production enhanced dose-dependently. Cell migration and invasion were also decreased by α-mangostin in OVACAR-3 cells. Finally, α-mangostin was observed to block the m-TOR/PI3K/AKT signaling pathway in OVACAR-3 cells.
Conclusion: α-Mangostin could induce antiproliferative effects against OVACAR-3 cells mediated via ROS production, mitochondrial-mediated apoptosis and inhibition of m-TOR/PI3K/AKT signalling. Therefore, it may prove a lead molecule in ovarian cancer treatment.
Oridonin triggers G2/M cell cycle arrest, cellular apoptosis and autophagy in human gastric cancer cells
Traditional Uyghur medicine Quercus infectoria galls water extract triggers apoptosis and autophagic cell death in colorectal cancer cells
Background: The water extract of Quercuse infectoria galls (QIG) is the active ingredient of Uyghur medicine Xipayi Kui Jie’an (KJA) which has promising therapeutic effects on Ulcerative Colitis (UC) as an alternative medicine. Considering the relationship between UC and the development of colorectal cancer (CRC), the present work aims to explore the direct anti-CRC activity of QIG extract.
Methods: CCK8 assay and flow cytometry were used to detect cytotoxicity and apoptosis. Transmission electron microscopy (TEM), flow cytometry, laser confocal and western blotting were performed to examine autophagy. We also adopted Reactive Oxygen Assay kit, as well as transwell and wound healing tests to study the underlying mechanism of QIG against CRC cells.
Results: First, we found that QIG extract could suppress the viability of CRC cells and trigger caspases-dependent apoptosis. Subsequently, we proved for the first time that QIG extract also triggered autophagic cell death in CRC cells, which together with apoptosis contributed to the cytotoxic effect on CRC cells. Further investigation revealed that QIG-induced cytotoxicity associated with intracellular ROS accumulation which could suppress the AKT/mTOR signaling pathway, and then induce autophagy and inhibit cell growth. Besides, Erk signaling pathway was also involved in the process of autophagic cell death. Moreover, QIG extract also influenced EMT process and inhibited CRC cell migration.
IgG Antibody (Rabbit anti Goat) (Fc) was previously known under catalogue number 18-511-244198 was previously known under catalogue number 18-511-244198
IgG Antibody (Goat anti Rabbit) (H&L) was previously known under catalogue number 18-511-244256 was previously known under catalogue number 18-511-244256
IgG Antibody (Goat anti Rabbit) (H&L) was previously known under catalogue number 18-511-244257 was previously known under catalogue number 18-511-244257
IgG Antibody (Goat anti Rabbit) (H&L) was previously known under catalogue number 18-511-244202 was previously known under catalogue number 18-511-244202
IgG Antibody (Goat anti Rabbit) (H&L) was previously known under catalogue number 18-511-244324 was previously known under catalogue number 18-511-244324
IgG Antibody (Goat anti Rabbit) (H&L) was previously known under catalogue number 18-511-244213 was previously known under catalogue number 18-511-244213
IgG Antibody (Goat anti Rabbit) (H&L) was previously known under catalogue number 18-511-244236 was previously known under catalogue number 18-511-244236
IgG Antibody (Goat anti Rabbit) (H&L) was previously known under catalogue number 18-511-244326 was previously known under catalogue number 18-511-244326
Lyophilized powder containing 10 mM Sodium Phosphate, 0.15 M Sodium Chloride, 1% (w/v) BSA and 0.1% (v/v) Kathon CG. Protease/IgG free, pH 7.2. Rehydrate with 1.1 ml of deionized water. Prepare fresh working dilution daily.
Description: Goat anti Rabbit IgG secondary antibody (HRP)
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