scholarly journals PHYTOCEMICALS SCREENING AND CELL CYCLE ARREST ACTIVITY OF n-HEXANE EXTRACT OF Vernonia amygdalina Delile LEAVES AGAINST PANCREATIC CANCER CELL LINE

2019 ◽  
Vol 7 (4) ◽  
pp. 12-16
Author(s):  
M L Fauzan ◽  
P A Z Hasibuan ◽  
U Harahap
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Pancreatic Cancer Cell Line ◽  
Hexane Extract ◽  
Assay Method ◽  
Vernonia Amygdalina ◽  
M1 Phase ◽  
Cycle Arrest ◽  
Apoptosis Process ◽  
Arrest Activity

Objective: This study aims to determined phytochemical compounds of simplex and n-hexane extract (nHE) of Vernonia amygdalina Delile Leaves and cell cycle arrest activity against PANC-1 cells. Methods: The leaves of Vernonia amygdalina Delile were dried and extracted with n-hexane, followed by evaporation and freeze-drying. Phytochemicals screening were analyzed with standard procedures. Cytotoxic activity was carried out using MTT assay method. PANC-1 cells were treated with different concentrations of nHE (500 ug/mL, 250 ug/mL, 125 ug/mL, 61.5 ug/mL and 31.25 ug/mL) for 24 hours to obtained IC50 values. The cell cycle inhibition activity of nHE was carried out used flowcytometry method and apoptosis activity used double staining method. Results: Then HE was identified contains steroids/triterpenoids. The IC50 was114.80 ± 1.21 ug/mL. The nHE inhibited cell cycle PANC-1 on M1 phase (67.39%) and it was induced apoptosis process on PANC-1 cells. Conclusions: Our results suggest that extractsn­-hexane of Vernonia amygdalina Delile Leaves had as cancer chemoprevention activities with inhibits cell cycle and spur apoptosis process on PANC-1 cells.   Keywords: 

PHYTOCHEMICALS ANALYSIS AND CELL CYCLE ARREST ACTIVITY OF ETHANOL EXTRACT OF Litsea cubeba Lour. FRUITS TOWARDS MCF-7/HER-2 CELL LINE

2021 ◽  
Vol 14 (01) ◽  
pp. 16-18
Author(s):  
Aminah Dalimunthe ◽  
Poppy Anjelisa Zaitun Hasibuan ◽  
Muflihah Fujiko ◽  
Masfria ◽  
Denny Satria
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cell Line ◽  
Ethanol Extract ◽  
Litsea Cubeba ◽  
Cycle Arrest ◽  
Her 2 ◽  
Arrest Activity ◽  
Mcf 7

scholarly journals Retama monosperma n-hexane extract induces cell cycle arrest and extrinsic pathway-dependent apoptosis in Jurkat cells

2014 ◽  
Vol 14 (1) ◽  
Author(s):  
Lamiae Belayachi ◽  
Clara Aceves-Luquero ◽  
Nawel Merghoub ◽  
Youssef Bakri ◽  
Silvia Fernández de Mattos ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Hexane Extract ◽  
Jurkat Cells ◽  
Extrinsic Pathway ◽  
Cycle Arrest ◽  
Retama Monosperma

scholarly journals CELL CYCLE ARREST ACTIVITY OF LITSEA CUBEBA LOUR: HEARTWOOD AND FRUIT EXTRACTS AGAINST T47D BREAST CANCER CELLS

2017 ◽  
Vol 10 (11) ◽  
pp. 404 ◽  
Author(s):  
Aminah Dalimunthe ◽  
Poppy Anjelisa Z Hasibuan ◽  
Denny Satria
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Breast Cancer Cells ◽  
Inhibitory Concentration ◽  
Litsea Cubeba ◽  
Cycle Arrest ◽  
Ic50 Value ◽  
Ic50 Values ◽  
Diphenyl Tetrazolium Bromide ◽  
Arrest Activity

  Objective: This study was carried out to investigate cell cycle arrest activity toward T47D cells of Litsea cubeba heartwoods and fruits extract.Methods: Dry extracts were prepared from dry-grounded heartwoods and fruits by cold maceration using n-hexane, ethylacetate, and ethanol solvent. Cytotoxic activity were measured by [3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromide] methods and interpreted with inhibitory concentration 50% (IC50) value. Cell cycle arrest was investigated by flowcytometry method.Results: IC50 values for each n-hexane, ethylacetate, and ethanol of L. cubeba heartwoods and fruits were 76.34±2.61; 67.52±2.45; 71.23±2.37; 75.59±3.24; 162.58±15.08; 63.70±2.67 μg/mL, respectively. Cell cycle arrest for ethylacetate extract of heartwoods and fruits were accumulated in G0/G1 phase (56.70% and 65.56%).Conclusion: These results suggest that L. cubeba heartwoods and fruits has cell cycle arrest activity.

Hypoxia-induced p21waf and p27 regulation in c-myc immortalized cells

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 21125-21125
Author(s):  
M. Rosati ◽  
C. Raimondi ◽  
M. Di Seri
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Kinase Inhibitors ◽  
Proteasome Inhibitors ◽  
Fibroblast Cell ◽  
Resistance Mechanisms ◽  
Assay Method ◽  
Induce Cell Cycle Arrest ◽  
Cycle Arrest

21125 Background: Hypoxia is an adaptative response to tissue damage whose mechanisms have not been yet characterized. From a clinical viewpoint, tumours with more necrosis, an indicator of severe hypoxic stress, are often resistant to conventional treatment. Moreover, numerous tumours overexpressed c-myc which strongly enforces proliferation in oxygen deprived conditions. Evidences showed that c-myc blocked cyclin-dependent kinase inhibitors (CDKI) through a complex network of interactions inducing proliferation and G0-S transition. We examined whether Rat-1 immortalized fibroblasts underwent cell cycle arrest p21waf- and p27- mediated in response to O2-deprivation. Materials and Methods: c-myc null cells (-/-) were derived by gene targeting from an immortalized but otherwise non- transformed Rat-1 fibroblast cell line. Oxygen deprivation conditions (0.2% and 1% O2) were achieved in a humidified anaerobic workstation at 37 °C for 6 or 24 hours. Protein concentration was determined by the Lawry assay method. Immunoblots for c-myc and p21waf and p27 were performed. Results: c-myc (+/+) samples collected after 6 hours of hypoxia, which were supposed to be slowly proliferating, showed lower p21waf and p27 levels than c-myc (-/-). Over 24 hours of hypoxia, cell cultures were supposed to be oxygen-dependent and we found higher CDKI levels in c-myc (+/+) cells. Discussion: Our data could explain same resistance mechanisms of tumours cells. In fact, 6 hours O2-deprived-cells, which are unable to supply autonomous O2 support (neo-angiogenesis, in vivo), downregulated p21waf and p27 expression to overcome CDKI cell-cycle arrest. When the cells acquired O2-dependent growth mechanism, low O2 level induced c-myc mediated p21waf and p27 up-regulation to induce cell cycle arrest. Despite the up-regulation of CDKI, PS 341 (a proteasome inhibitors) has been demonstrated to induce apoptosis. Our data kindly encouraging trials on the use of p21waf and p27 stabilizers (like PS 341) in those tumours which overexpressed c-myc. No significant financial relationships to disclose.

scholarly journals The Anti-Proliferation, Cycle Arrest and Apoptotic Inducing Activity of Peperomin E on Prostate Cancer PC-3 Cell Line

Molecules ◽  
2019 ◽  
Vol 24 (8) ◽  
pp. 1472 ◽  
Author(s):  
Yunzhi Li ◽  
Jigang Pan ◽  
Meng Gou
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cell Line ◽  
Cell Lines ◽  
Caspase 3 ◽  
Proliferation Inhibition ◽  
Cycle Arrest ◽  
Regulated Expression ◽  
Arrest Activity

Peperomin E is a natural secolignan existing distributed in the plants of the genus Peperomia. Previous investigations demonstrated that peperomin E showed potential antitumor activity in some cancer lines, but it is unclear whether peperomin E has an effect on prostate cancer cell lines. The aim of the present study is to investigate its effects on proliferation inhibition, apoptosis-inducing and cell-cycle arrest activity using a prostate cancer PC-3 cell line. The proliferation inhibition was evaluated by MTT assay, apoptosis was detected by Annexin V/propidium iodide (PI) staining and Hoechst 33258 staining, cell cycle distributions were measured by flow cytometry, and western blot analysis was used to determine specific cellular apoptotic protein expressions of Bcl-2, Bax, caspase-3 and cleaved-caspase-3. According to the results of this study, peperomin E exhibited significant anti-proliferation activity on PC-3 cell lines in vitro in a dose-dependent manner. Peperomin E treatments lead to marked morphological changes. Apoptotic cell count and cell-cycle distribution at G2/M phase significantly increased with increasing concentrations of peperomin E. The down-regulated expression level of Bcl-2 and up-regulated expression level of Bax and cleaved-caspase-3 compared with the controls were also observed after peperomin E treatment. These data suggest that peperomin E exhibited proliferation inhabitation, apoptosis-inducing and cell-cycle arrest activity on PC-3 cell lines. The anti-proliferation effect of peperomin E on PC-3 cells should result partly from its cell-cycle arrest and apoptosis-inducing activity, whereas the increasing of the Bax/Bcl-2 ratio and activation of caspases-3 play an important role in the development of apoptosis.

Algerian Propolis Potentiates Doxorubicin Mediated Anticancer Effect Against Human Pancreatic PANC-1 Cancer Cell Line through Cell Cycle Arrest, Apoptosis Induction and P-Glycoprotein Inhibition

2018 ◽  
Vol 18 (3) ◽  
pp. 375-387 ◽  
Author(s):  
Hassiba Rouibah ◽  
Wided Kebsa ◽  
Mesbah Lahouel ◽  
Malek Zihlif ◽  
Mamoun Ahram ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Cell Cycle Arrest ◽  
Cell Line ◽  
Cancer Cell ◽  
Antitumor Effect ◽  
Pancreatic Cancer Cell ◽  
Pancreatic Cancer Cell Line ◽  
Cancer Cell Line ◽  
Cycle Arrest

Background: Pancreatic cancer is one of the most aggressive and lethal cancers, with poor prognosis and high resistance to current chemotherapeutic agents. Therefore, new therapeutic strategies and targets are underscored. Propolis has been reported to exhibit a broad spectrum of biological activities including anticancer activity. Objective: This study was carried out to assess the possible efficacy of Algerian propolis on the antitumor effect of doxorubicin on human pancreatic cancer cell line (PANC-1). Methods: Modifications in cell viability, apoptosis and cell cycle progression, Pgp activity and intracellular accumulation of DOX were monitored to study the synergistic effect of Algerian propolis on the antitumor effects of DOX in PANC-1 cell line. Results: Both propolis and its combination with doxorubicin inhibited cell growth in a dose-dependent manner by inducing cell cycle arrest and apoptosis. In the presence of 100 μg/ml of propolis, the IC50 of DOX against PANC-1 cells decreased by 10.9-fold. Propolis combined with DOX increased after 48h, the number of cells in the G0G1 phase with dramatical increase in sub-G1 phase to reach 47% of total cells, corresponding to an increase of senescence or apoptotic state of the cells. Dead cell assay with annexinV/PI staining demonstrated that propolis and propolis-DOX treatment resulted in a remarkable induction of apoptosis as detected by flow cytometry. It was interesting to note that propolis at its 5IC50 was found as the most potent inducer of apoptosis. Our finding revealed that induced apoptosis in our conditions was caspase-3 and caspase-9 dependent. Flow cytometry showed that propolis increased the accumulation of doxorubicin within PANC-1 cells. Moreover, fluorescent intensity detection revealed that propolis remarkably increased the retention of rhodamine-123, 7- fold compared to 3-fold of verapamil, the most effective P-gp inhibitor. Conclusion: In conclusion, propolis sensitize pancreatic cancer cells to DOX via enhancing the intracellular retention of DOX due to blocking the efflux activity of P-gp pump, inducing cell cycle arrest and increasing apoptosis, finding that improuve the synergism of antitumor effect of Algerian propolis and DOX in pancreatic cancer cell line. Therefore, Algerian propolis may be an effective agent in a combined treatment with doxorubicin for increased therapeutic efficacy against pancreatic cancer.

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