Lee, Sun Min;Kim, Young Sook;Jang, Wook Jin;Rakib, Abdur Md.;Oh, Tae Woo;Kim, Boh Hyun;Kim, So Young;Kim, Jeong Ok;Ha, Yeong Lae
Journal of Life Science
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v.23
no.11
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pp.1351-1359
/
2013
The anti-proliferative activity of ${\beta}$-ionone was investigated on human non-small lung cancer A-549 cells (designated A-549 cells). A-549 cells were treated with various concentrations of ${\beta}$-ionone (1, 5, 10, and 15 ${\mu}M$) for two, four, and six days. Biochemical markers related to the growth inhibition of A-549 cells by ${\beta}$-ionone were measured at the second day of incubation. ${\beta}$-Ionone inhibited the growth of A-549 cells by dose-and time-dependent manners, resulting in an $IC_{50}$ of 5.0 ${\mu}g/ml$ at the second day of incubation. ${\beta}$-Ionone induced apoptosis by a dose-dependent manner. ${\beta}$-Ionone increased levels of p53, p21, and Bax proteins, but suppressed expression of the Bcl-2 protein. Similarly, ${\beta}$-ionone enhanced cytochrome c release from the mitochondria to the cytosol, and induced activation of caspase-9 and -3. Additionally, ${\beta}$-ion-one reduced $cPLA_2$ and COX-2 protein levels. These results suggest that the ${\beta}$-ionone inhibits the proliferation of A-549 cells through reciprocal regulation of Bax and Bcl-2 gene expression and suppression of $cPLA_2$ and COX-2 protein expressions.
The methanol extract from the aerial parts of Aceriphyllum rossii was fractionated into ethyl acetate, n-BuOH and $H_2O$ layers through solvent fractionation. Repeated silica gel column chromatography of EtOAc and n-BuOH layers afforded five flavonol glycosides. They were identified as astragalin (1), kaempferol 3-O-${\alpha}$-L-rhamnopyranosyl (1${\rightarrow}$6)-${\beta}$-D-glucopyranoside (2), rutin (3), kaempferol 3-O-${\alpha}$-L-rhamnopyranosyl (1${\rightarrow}$4)-${\alpha}$-L-rhamnopyranosyl 1${\rightarrow}$6)-${\beta}$-D-glucopyranoside (4), and quercetin 3-O-${\alpha}$-L-rhamnopyranosyl (1${\rightarrow}$4)-${\alpha}$-L-rhamnopyranosyl (1${\rightarrow}$6)-${\beta}$-D-glucopyranoside (5) on the basis of spectroscopic data. All of them showed an inhibition in farnesyl protein tranferase (FPTase) activity, and rutin (3) inhibited the growth of rat H-ras cell and the cell migration of human umbilical vein endothelial cells (HUVECs).
In order to investigate whether SKI-II could reverse drug resistance and its possible mechanisms, we treated SGC7901/DDP cells with SKI-II or SKI-II in combination with DDP. Then cell growth, apoptosis, micromorphological changes, and expression of SphK1, P-gp, NF-${\kappa}B$, Bcl-2 and Bax were assessed by MTT assay, flow cytometry, electron microscopy, immunocytochemistry and Western blot assay respectively. SGC7901/DDP cells were insensitive to cisplatin 2.5mg/L, but when pretreated with SKI-II, their proliferation was inhibited by cisplatin 2.5mg/L significantly, the inhibition rate increasing with time and dose. The apoptosis rate was also significantly elevated. Expression of SphK1 and P-gp was decreased significantly, Pearson correlation analysis showing significant correlation between the two (r=0.595, P<0.01). Expression of NF-${\kappa}B$ and Bcl-2 was decreased significantly,while that of Bax was increased, compared to the control group. There were significant correlations between SphK1 and NF-${\kappa}B$(r=0.723, P<0.01), NF-${\kappa}B$ and Bcl-2(r=0.768, P<0.01). All these data indicated that SKI-II could reverse drug resistance of SGC7901/DDP to cisplatin by down-regulating expression of P-gp and up-regulating apoptosis through down-regulation of SphK1. The increased apoptotic sensitivity of SGC7901/DDP to cisplatin was due to the decreasing proportion of Bcl-2/Bax via down-regulating NF-${\kappa}B$.
Fucoidan, a natural component of brown seaweed, has various biological activities such as anti-cancer activity, anti-oxidant, and anti-inflammatory against various cancer cells. However, the fucoidan has been implicated in melanoma cells via apoptosis signaling pathway. Therefore, we investigated apoptosis with fucoidan in A2058 human melanoma cells with dose- and time-dependent manners. In our results, A2058 cells viability decreased at relatively short-time and low-concentration through fucoidan. This effects of fucoidan on A2058 cells appeared to be mediated by the induction of apoptosis, as manifested by morphological changes through DNA-binding dye Hoechst 33342 staining. When a dose of 80 ㎍/mL fucoidan was treated, the cells were observed: crescent or ring-like structure, chromatin condensation, and nuclear fragmentation. With the increase at 100 ㎍/mL fucoidan, the cell membrane is intact throughout the total process, including membrane blebbing and loss of membrane integrity as well as increase of sub-G1 DNA. Furthermore, to understand the exact mechanism of fucoidan-treated in A2058 cells, western blotting was performed to detect apoptosis-related protein expression. In this study, Bcl-2 family proteins can be regulated by fucoidan, suggesting that fucoidan-induced apoptosis is modulated by intrinsic pathway. Therefore, expression of Bcl-2 and Bax may result in altered permeability, activating caspase-3 and caspase-9. And the cleaved form of poly ADP-ribose polymerase was detected in fucoidan-treated A2058 cells. These results suggest that A2058 cells are highly sensitive to growth inhibition by fucoidan via apoptosis, as evidenced by activation of extracellular signal-regulated kinases/p38/Bcl-2 family signaling, as well as alteration in caspase-9 and caspase-3.
Barghi, Leila;Asgari, Davoud;Barar, Jaleh;Nakhlband, Aylar;Valizadeh, Hadi
Asian Pacific Journal of Cancer Prevention
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v.15
no.23
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pp.10281-10287
/
2015
Background: Development of a nanosized polymeric delivery system for erlotinib was the main objective of this research. Materials and Methods: Poly caprolactone-polyethylene glycol-polycaprolactone (PCEC) copolymers with different compositions were synthesized via ring opening polymerization. Formation of triblock copolymers was confirmed by HNMR as well as FT-IR. Erlotinib loaded nanoparticles were prepared by means of synthesized copolymers with solvent displacement method. Results: Physicochemical properties of obtained polymeric nanoparticles were dependent on composition of used copolymers. Size of particles was decreased with decreasing the PCL/PEG molar ratio in used copolymers. Encapsulation efficiency of prepared formulations was declined by decreasing their particle size. Drug release behavior from the prepared nanoparticles exhibited a sustained pattern without a burst release. From the release profiles, it can be found that erlotinib release rate from polymeric nanoparticles is decreased by increase of CL/PEG molar ratio of prepared block copolymers. Based on MTT assay results, cell growth inhibition of erlotinib has a dose and time dependent pattern. After 72 hours of exposure, the 50% inhibitory concentration (IC50) of erlotinib hydrochloride was appeared to be $14.8{\mu}M$. Conclusions: From the obtained results, it can be concluded that the prepared PCEC nanoparticles in this study might have the potential to be considered as delivery system for erlotinib.
The purpose of this study was to evaluate the inhibitory effect of commercial Makgeolli on tumor growth in human gastric adenocarcinoma cells (AGS) in a xenograft cancer model, transplanted with AGS cells. Commercial Makgeolli was first dealcoholized by evaporation and used as the test sample. We detected a significant increase in the volume and weight of tumor in nude mice (induction) that were transplanted with AGS cells. Administration of $100mg/kg{\cdot}day$ group (ML), and $500mg/kg{\cdot}day$ group (MH) dealcoholized commercial Makgeolli significantly decreased tumor growth. In this study, 5-FU $18mg/kg{\cdot}day$ was used as a positive control for tumor growth inhibition. Additionally, determination of the body weight of both the groups revealed no side effects after the administration of dealcoholized commercial Makgeolli. Using the cell culture system, we also evaluated the effect of dealcoholized commercial Makgeolli on caspase-3/7 activity in the AGS cells. Treatment with dealcoholized commercial Makgeolli increased the activation of caspase-3/7 and the apoptotic markers in AGS cells in a dose-dependent manner. Therefore, dealcoholized commercial Makgeolli can be used for cancer prevention.
Objective : EID3 (EP300-interacting inhibitor of differentiation) was identified as a novel member of EID family and plays a pivotal role in colorectal cancer development. However, its role in glioma remained elusive. In current study, we identified EID3 as a novel oncogenic molecule in human glioma and is critical for glioma cell survival, proliferation and invasion. Methods : A total of five patients with glioma were recruited in present study and fresh glioma samples were removed from patients. Four weeks old male non-obese diabetic severe combined immune deficiency (NOD/SCID) mice were used as transplant recipient models. The subcutaneous tumor size was calculated and recorded every week with vernier caliper. EID3 and AMP-activated protein kinase α1 (AMPKα1) expression levels were confirmed by real-time polymerase chain reaction and Western blot assays. Colony formation assays were performed to evaluate cell proliferation. Methyl thiazolyl tetrazolium (MTT) assays were performed for cell viability assessment. Trypan blue staining approach was applied for cell death assessment. Cell Apoptosis DNA ELISA Detection Kit was used for apoptosis assessment. Results : EID3 was preferentially expressed in glioma tissues/cells, while undetectable in astrocytes, neuronal cells, or normal brain tissues. EID3 knocking down significantly hindered glioma cell proliferation and invasion, as well as induced reduction of cell viability, apoptosis and cell death. EID3 knocking down also greatly inhibited tumor growth in SCID mice. Knocking down of AMPKα1 could effectively rescue glioma cells from apoptosis and cell death caused by EID3 absence, indicating that AMPKα1 acted as a key downstream regulator of EID3 and mediated suppression effects caused by EID3 knocking down inhibition. These findings were confirmed in glioma cells generated patient-derived xenograft models. AMPKα1 protein levels were affected by MG132 treatment in glioma, which suggested EID3 might down regulate AMPKα1 through protein degradation. Conclusion : Collectively, our study demonstrated that EID3 promoted glioma cell proliferation and survival by inhibiting AMPKα1 expression. Targeting EID3 might represent a promising strategy for treating glioma.
Curcumin has diverse anticancer activities that lead to tumor growth inhibition of cancer cells and induction of apoptosis. Curcumin is involved in the regulation of multiple genes via transcription factors including NF-${\kappa}B$, STATs, AP1, and SP. Notch signaling plays critical roles in maintaining the balance between cell proliferation, differentiation and apoptosis, and thereby may contribute to the development of various cancers involving breast cancer. This study was to investigate the effects of curcumin on Notch1 gene expression and to explore the underlying mechanism. Here, we found that curcumin decreased the levels of Notch1 mRNA and protein in MDA-MB-231 human breast cancer cells, along with the downregulation of Sp family genes (Sp1, Sp2, Sp3, and Sp4). The repressive effect of curcumin on Notch1 gene transcription was confirmed by performing Notch1 promoter-driven reporter assay and three Sp-binding sites were identified on Notch1 promoter that may act as curcumin-respose elements. Moreover, treatment with mitramycin A, a specific Sp inhibitor, decreased the levels of Notch1 mRNA and protein in human breast cancer cells. Taken together, our results indicate that Notch1 gene expression is downregulated by curcumin, at least in part, through the suppression of Sp family, which may lead to apoptosis in human breast cancer cells.
Sorghum bicolor L. is one of the important minor cereals in Asia, Africa, and the central United States, and it is considered a rich source of polyphenols, flavonoids, and dietary fiber. However, there is a lack of data on the anti-cancer activity of Sorghum in prostate cancer cells and immune activity in macrophages. This study aims to investigate the potential effects of an ethanol extract of S. bicolor L. (SE) on inducing apoptosis in RC-58T/h/SA#4 cells and immunomodulatory activity in RAW 264.7 cells. SE significantly inhibited the viability of RC-58T/h/SA#4 primary prostate cancer cells in a dose-dependent manner. The morphology of RC-58T/h/SA#4 cells treated with SE was shrunken and involved the formation of an apoptotic body and nuclear condensation. In addition, SE markedly activated caspase-8, -9, and -3; increased the protein levels of Bax, p53, cleaved PARP, and cytosolic cytochrome c; and decreased Bcl-2 protein expression. Furthermore, the inhibition of caspases in RC-58T/h/SA#4 cells with z-VAD-fmk attenuated SE-induced cell growth inhibition. The production of nitric oxide (NO) was also elevated by SE treatment, as revealed by immune response parameters. These results suggest that SE inhibits growth and induces apoptosis in primary human prostate cancer cells in a caspase-dependent manner, and it modulates the immune functions in macrophages. Therefore, Sorghum bicolor L. may be used as a functional food to prevent prostate cancer and enhance immune activity.
This experiment was conducted to obtain the have higher contents of pharmaceutical constituents as well as higher yield from colchicine induced diploid and tetraploid extracts of Platycodon grandiflorum. In order to determine the biological activity, this study was focused to evaluate the cytotoxicity, antimicrobial on the bronthus disease bacteria, antioxidant enzyme activity of diploid and tetraploid extracts in P. grandiflorum. The activities of antioxidant enzyme according to different solvent extracts were measured as superoxide dismutase (SOD), catalase (CAT), peroxidase (POD), and ascorbate peroxidase (APX). The cytotoxicity of methanol extracts of P. grandiflorum showed significant differences between tetraploid and diploid. That is, the cytotoxic effect against human cancer cell was higher in tetraploid than in diploid. At all extracts concentration, tetraploid samples showed high toxicity and the $IC_{50}$ (concentration causing 50% cell death) value showed the highest on HCT-116 cell ($105.91{\mu}g/mL$), and exhibited significant activity against the Hep 3B cell ($140.67{\mu}g/mL$), SNU-1066 cell ($154.01{\mu}g/mL$), Hela cell ($158.37{\mu}g/mL$), SNU-601 cell ($182.67{\mu}g/mL$), Calu-6 cell ($190.42{\mu}g/mL$), MCF-7 cell ($510.19{\mu}g/mL$). Antimicrobial activities of diploid P. grandiflorum were relatively low compared to tetraploid P. grandiflorum on most of the bacterial strains. In tetraploid P. grandiflorum, K. pneumoniae showed the clear zone formation (18~19 mm) of growth inhibition, followed by the clear zone formation of 13~15 mm on C. diphtheria and S. pyogenes. The antimicrobial activities in diploid P. grandiflorum were the highest on K. pneumonia (14~15 mm), and showed the clear zone formation of 11~12 mm on C. diphtheria and 12~13 mm on S. pyogenes. The antimicrobial activity is thought to look different depending on the bacterial strains and the polyploidy of P. grandiflorum. The root extract of P. grandiflorum had the highest (97.2%) SOD enzyme activity in ethyl acetate partition layer of tetraploid while water partition layer of diploid showed the lowest (48.6%) SOD enzyme activity. The activity of CAT showed higher values in the root of tetraploid than in the diploid of P. grandiflorum in all partition layers except butyl alcohol. The activities of APX and POD showed higher values in the root of tetraploid than in the diploid of P. grandiflorum in all fraction solvents except water layer. These results indicate that the tetraploid P. grandiflorum can be used as a source for developing cytotoxic agent and antimicrobials which can act against bronchus diseases bacterial strains.
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