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extract inhibits hepatocellular carcinoma via induction of caspase-dependent apoptosis.

Cancer is a disease with a global burden and is a major and increasing threat to public health. The demand for new modalities to treat and prevent cancer is high. Given the toxic side effects of standard treatments, such as chemotherapy, there is greater research interest in naturally derived compounds due to their selective toxicity to cancer cells. This study aimed to test the anticancer activity of a crude extract ofon hepatocellular carcinoma (HCC) HepG2 cell line.

2560 related Products with: extract inhibits hepatocellular carcinoma via induction of caspase-dependent apoptosis.

Cell Meter™ Caspase 3 7 Cell Meter™ Caspase 3 7 Cell Meter™ Caspase 3 7 Cell Meter™ Caspase 8 A Cell Meter™ Caspase 9 A Cell Meter™ Caspase 9 A Cell Meter™ Caspase 9 A Cell Meter™ Caspase 8 A Cell Meter™ Caspase 9 A Hepatocellular carcinoma Hepatocellular carcinoma Hepatocellular carcinoma

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Chloro(triphenylphosphine)gold(I) a forefront reagent in gold chemistry as apoptotic agent for cancer cells.

The antiproliferative activity of the gold complex [Au(tpp)Cl] (1) (tpp=triphenyphosphine) against human breast adenocarcinoma cells (MCF-7) and normal human fetal lung fibroblast cells (MRC-5) was investigated. The compound exhibits stronger activity against MCF-7 cells than cisplatin. The apoptotic pathway, especially though the mitochondrion damage was concluded by cell cycle arrest, flow cytometry using Annexin V-Fluorescein IsoThioCyanate (FITC) and Propidium Iodide (PI) as indicators, assays and permeabilization of the mitochondrial membrane tests. The molecular mechanism of action of 1 was further studied by: (i) its catalytic activity on the oxidation of linoleic acid (an acid that partakes in membrane fluidity) to hyperoxolinoleic acid by oxygen and (ii) its binding affinity towards the calf thymus (CT) DNA. Since the deactivation of cisplatin by glutathione (GSH), is related with the development of cell resistance, the reaction of 1 with GSH was investigated by UV absorption spectroscopy. The absence of micronucleus in cells confirms that the complex has no in vitro toxicity. The in vivo genotoxicity caused by 1 was evaluated by Allium cepa test.

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Melatonin-Induced Changes in Cytosolic Calcium Might be Responsible for Apoptosis Induction in Tumour Cells.

Melatonin is a hormone transferring information about duration of darkness to the organism and is known to modulate several signaling pathways in the cells, e.g. generation of endoplasmic reticulum stress, oxidative status of the cells, etc. Melatonin has been shown to exert antiproliferative and cytotoxic effects on various human cancers. We proposed that this hormone can differently affect tumour cells and healthy cells.

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Inhibition of autophagy attenuated curcumol-induced apoptosis in MG-63 human osteosarcoma cells via Janus kinase signaling pathway.

The present study aimed to investigate whether autophagy was triggered by curcumol and to explore the association between autophagy and apoptosis of MG-63 cells and the underlying mechanism. MG-63 cells were cultured. An MTT assay was performed to evaluate the proliferation inhibition of the MG-63 osteosarcoma cell line by curcumol. Fluorescein isothiocyanate-Annexin V/propidium iodide staining flow cytometry was performed to analyze the apoptotic rate of cells. The morphological alterations of cell nuclei were evaluated by Hoechst 33258 viable cell staining. The effects of autophagy in cells was investigated by green fluorescent protein (GFP)-light chain 3 (LC3) transfection and using a fluorescence microscope. The expression levels of LC3II, LC3I and cleaved caspase-3 and Janus kinase (JNK) signaling pathway activation were determined by western blot analysis. Cell proliferation was inhibited by curcumol in a dose- and time-dependent manner. Curcumol induced apoptosis by the caspase-dependent signaling pathway in MG-63 cells. The present study demonstrated that curcumol could induce autophagy of MG-63 cells, which was evaluated by transmission electron microscopy. Compared with the curcumol treatment alone group, the GFP-LC3-transfected green fluorescence plasmids and the LC3II/LC3I levels in cells of the curcumol and chloroquine (CQ) treatment group were upregulated, and the apoptotic ratio was downregulated following pretreatment with autophagy inhibitor CQ for 1 h. Furthermore, curcumol treatment induced phosphorylation of the JNK signaling pathway. Of note, pretreatment with the JNK inhibitor, SP600125, decreased the rates of autophagy and apoptosis, suggesting a crucial role served by the JNK signaling pathway in the activation of autophagy by curcumol. Taken together, the results of the present study suggested that activation of the JNK signaling pathway was involved in curcumol-induced autophagy. Curcumol is a novel drug for chemotherapeutic combination therapy. Curcumol demonstrated potential antitumor activities in MG-63 cells and may be used as a novel effective reagent in the treatment of osteosarcoma.

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Cytotoxicity of Dental Implants: The Effects of Ultrastructural Elements.

In this in vitro study, the purpose was to assess the cytotoxicity profiles of seven commercial dental implant materials by using cell culture methods on an osteoblastic cell line.

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Modulating lysosomal function through lysosome membrane permeabilization or autophagy suppression restores sensitivity to cisplatin in refractory non-small-cell lung cancer cells.

Lung cancer is the leading cause of cancer-related deaths. Most patients develop resistance to platinum within several months of treatment. We investigated whether triggering lysosomal membrane permeabilization (LMP) or suppressing autophagy can restore cisplatin susceptibility in lung cancer with acquired chemoresistance. Cisplatin IC50 in A549Pt (parental) and A549cisR (cisplatin resistant) cells was 13 μM and 47 μM, respectively. Following cisplatin exposure, A549cisR cells failed to elicit an apoptotic response. This was manifested by diminished Annexin-V staining, caspase 3 and 9, BAX and BAK activation in resistant but not in parental cells. Chloroquine preferentially promoted LMP in A549cisR cells, revealed by leakage of FITC-dextran into the cytosol as detected by immunofluorescence microscopy. This was confirmed by increased cytosolic cathepsin D signal on Immunoblot. Cell viability of cisplatin-treated A549cisR cells was decreased when co-treated with chloroquine, corresponding to a combination index below 0.8, suggesting synergism between the two drugs. Notably, chloroquine activated the mitochondrial cell death pathway as indicated by increase in caspase 9 activity. Interestingly, inhibition of lysosomal proteases using E64 conferred cytoprotection against cisplatin and chloroquine co-treatment, suggesting that chloroquine-induced cell death occurred in a cathepsin-mediated mechanism. Likewise, blockage of caspases partially rescued A549cisR cells against the cytotoxicity of cisplatin and chloroquine combination. Cisplatin promoted a dose-dependent autophagic flux induction preferentially in A549cisR cells, as evidenced by a surge in LC3-II/α-tubulin following pre-treatment with E64 and increase in p62 degradation. Compared to untreated cells, cisplatin induced an increase in cyto-ID-loaded autophagosomes in A549cisR cells that was further amplified by chloroquine, pointing toward autophagic flux activation by cisplatin. Interestingly, this effect was less pronounced in A549Pt cells. Blocking autophagy by ATG5 depletion using siRNA markedly enhances susceptibility to cisplatin in A549cisR cells. Taken together, our results underscore the utility of targeting lysosomal function in overcoming acquired cisplatin refractoriness in lung cancer.

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Glucosylceramide synthase regulates the proliferation and apoptosis of liver cells in vitro by Bcl‑2/Bax pathway.

Our previous study found that glucosylceramide, a type of sphingolipids, was associated with liver inflammation and fibrosis. Glucosylceramide is generated by glucosylceramide synthase (GCS), which is encoded by the UDP‑glucose ceramide glucosyltransferase (UGCG) gene. GCS is a key enzyme to regulate the physiological activity of cells. However, the role of GCS in hepatic cells remains unclear. The aim of the present study was to explore the mechanism of GCS in the proliferation and apoptosis of liver cells. Following the interference of expression of GCS in vitro by UGCG small interfering (si)RNA, the MTT method was performed to detect the proliferation of HL‑7702 hepatocytes, and ELISA was used to determine the concentration of tumor necrosis factor (TNF) α and cytochrome c in the supernatant of culture system. Fluorescence microscopy was used to observe the apoptosis of liver cells stained by Annexin V‑fluorescein isothiocyanate/propidium iodide. Reverse transcription‑quantitative polymerase chain reaction was used to detect the gene expression apoptosis regulator Bcl‑2 (Bcl‑2), apoptosis regulator Bax (Bax) and caspase-3. Western blot analysis was used to detect the expression of caspase-3 protein in the liver cells. Following treatment with UGCG siRNA for 24 h, the proliferation of HL‑7702 hepatocytes was significantly inhibited when compared with the transfection reagent group. Furthermore, the early and advanced apoptosis of liver cells showed an increasing trend. Additionally, concentrations of TNF α and cytochrome c showed no significant difference between the UGCG siRNA and transfection reagent groups. Compared with the transfection reagent group, Bcl‑2 mRNA expression decreased, and Bax and caspase-3 mRNA expression increased in the UGCG siRNA transfection group. The protein expression level of caspase-3 showed increased in hepatocytes following the treatment with UGCG siRNA. In conclusion, the metabolic changes of sphingolipids caused by the lack of GCS may be involved in the proliferation and apoptosis of liver cells through the Bcl‑2/Bax signaling pathway.

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Cytotoxic and Apoptogenic Effects of Cyanidin-3-Glucoside on the Glioblastoma Cell Line.

Glioblastoma multiforme (GBM) is the most prevalent and aggressive primary cerebral tumor. The median survival time is 15 months despite maximum treatment because the tumor is resistant to most therapeutic modalities. Several studies have indicated chemopreventive and chemotherapeutic activity of cyanidin-3-glucoside (C3G) as an anthocyanin component. We aimed to illustrate the cytotoxic and apoptogenic effects of C3G in the U87 cell line (human GBM cell line).

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DIFFERENT CONCENTRATIONS OF SIJUNZI DECOCTION INHIBIT PROLIFERATION AND INDUCE APOPTOSIS OF HUMAN GASTRIC CANCER SGC-7901 SIDE POPULATION.

Sijunzi Decoction (SD) is a traditional Chinese medicine which is composed of Ginseng, Atractylodes, Poria and Licorice. It is one of the commonly used Chinese traditional medicines that showed anti-gastric cancer activity in clinical studies. Previous evidence demonstrated SD parties (Ginseng, Atractylodes, Poria, Licorice) can inhibit proliferation and induced apoptosis for gastric cancer cell. In order to further investigate the anticancer effect of SD in gastric cancer, we observed the effects of different concentrations of SD on proliferation and apoptosis of Side Population Cells (SP) of human gastric cancer SGC-7901.

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Effect of the Diabetic Environment On the Expression of MiRNAs in Endothelial Cells: Mir-149-5p Restoration Ameliorates the High Glucose-Induced Expression of TNF-α and ER Stress Markers.

This study aimed to screen microRNAs and their corresponding target genes that are associated with vascular injury in type two diabetes mellitus (T2DM), investigate the effects of differentially expressed miRNAs and their target genes on high glucose-induced vascular injury and establish the mechanism underlying these effects.

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