scholarly journals Cytotoxicity of 9,11-Dehydroergosterol Peroxide Isolated from Ganoderma Lucidum and its Target-related Proteins

2010 ◽  
Vol 5 (8) ◽  
pp. 1934578X1000500 ◽  
Author(s):  
Ya-Jun Cui ◽  
Shu-Hong Guan ◽  
Li-Xing Feng ◽  
Xiao-Yi Song ◽  
Chao Ma ◽  
...  
Keyword(s):  
Hela Cells ◽  
Ganoderma Lucidum ◽  
Morphological Changes ◽  
Expression Profiles ◽  
Carcinoma Cells ◽  
Cellular Targets ◽  
Stathmin 1 ◽  
Induced Apoptosis ◽  
Protein Expression Profiles ◽  
Related Proteins

The cytotoxicty of 9,11-dehydroergosterol peroxide (DHEP) isolated from the fruiting bodies of Ganoderma lucidum on HeLa cells was studied. DHEP treatment for 48 h inhibited the proliferation of HeLa human cervical carcinoma cells with an IC50-value of 8.58 ± 0.98 μM. Morphological changes of DHEP-treated cells indicated that DHEP induced apoptosis in HeLa cells. To identify the cellular targets of DHEP, two-dimensional electrophoresis analysis was performed to compare the protein expression profiles of DHEP-treated cells with that of control cells. Proteins altered in expressional level after DHEP exposure were identified by MALDI-TOF MS/MS. The cytotoxic effect of DHEP was associated with regulated expression of 6 proteins. Stathmin 1 might be an important target-related protein of DHEP. The regulation of stathmin 1 by DHEP treatment was also confirmed by Western blotting.

scholarly journals Effects of Propofol on Several Membrane Characteristics of Cervical Cancer Cell Lines

2016 ◽  
Vol 40 (1-2) ◽  
pp. 172-182 ◽  
Author(s):  
Fan Zhang ◽  
Changsong Wang ◽  
Yinghua Cui ◽  
Shuping Li ◽  
Yuanfei Yao ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cell Membrane ◽  
Cervical Carcinoma ◽  
Hela Cells ◽  
Molecular Mechanisms ◽  
Morphological Changes ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Membrane Ultrastructure

Background: Although significant advances have been made toward understanding the molecular mechanisms underlying the effect of propofol on tumor cell metastasis, less is known regarding how cell membrane and cytoskeletal ultrastructure are affected in this process. Here, we investigated the relationship between cell morphology and cell size, which are features mainly defined by the cytoskeleton. Methods: To confirm the effects of propofol on the migratory ability of human cervical carcinoma cells, cell migration and invasion were examined through scratch wound healing and transwell membrane assays. Furthermore, HeLa cells cultivated with different concentrations of propofol were examined by confocal microscopy and atomic force microscopy (AFM), and the mean optical density and migration ability of these cells were also assessed. In addition, cell membrane morphology was inspected using AFM. Results: The results of the wound healing and transwell membrane assays indicated that propofol decreases the migratory ability of cervical carcinoma cells compared to control cells. A comparative analysis of the test results revealed that short-term (3 h) exposure to propofol induced marked changes in cell membrane microstructure and in the cytoskeleton in a dose-dependent manner. These morphological changes in the cell membrane were accompanied by cytoskeleton (F-actin) derangement. The present findings demonstrate a close relationship between changes in cell membrane ultrastructure and cytoskeletal alterations (F-actin) in propofol-treated HeLa cells. AFM scanning analysis showed that cell membrane ultrastructure was significantly changed, including a clear reduction in membrane roughness. Conclusion: The influence of propofol on the HeLa cell cytoskeleton can be directly reflected by changes in cellular morphology, as assessed by AFM. Moreover, the use of AFM is a good method for investigating propofol-mediated changes within cytoskeletal ultrastructure.

Anticancer activity and mechanism of juglone on human cervical carcinoma HeLa cells

2012 ◽  
Vol 90 (11) ◽  
pp. 1553-1558 ◽  
Author(s):  
Wei Zhang ◽  
Anheng Liu ◽  
Yan Li ◽  
Xingyu Zhao ◽  
Shijie Lv ◽  
...  
Keyword(s):  
Hela Cells ◽  
Morphological Changes ◽  
Annexin V ◽  
Chemical Constituent ◽  
Parp Cleavage ◽  
Dependent Manner ◽  
Transmission Electron ◽  
Major Chemical ◽  
Related Proteins ◽  
Dose Dependent

Induction of apoptosis in tumor cells has become the major focus of anti-tumor therapeutics development. Juglone, a major chemical constituent of Juglans mandshurica Maxim, possesses several bioactivities, including anti-tumor. In the present study, HeLa cells were incubated with juglone at various concentrations. The proliferation inhibition of juglone on HeLa cells was tested by the MTT assay. Occurrence of apoptosis was detected by Hoechst 33258 staining, flow cytometry, and transmission electron microscopy. The expression of apoptotic-related proteins was examined by Western blot. The results showed that juglone inhibits the growth of HeLa cells in dose–dependent manner. Topical morphological changes of apoptotic body formation after juglone treatment were observed. The percentages of early apoptosis of Annexin V-FITC were 5.23%, 7.95%, 10.69%, and 20.92% with the concentrations of juglone (12.5, 25, 50, and 100 µmol/L), respectively. After cells were treated with juglone at the different dose for 24 h, the expression of Bcl-2 was significantly down-regulated and the expression of Bax was significantly up-regulated compared with the control. These events paralleled with activation of caspase-9, -8, -3, and PARP cleavage. The results suggest that juglone may be effective for the treatment of HeLa cells.

scholarly journals Immunomodulatory Effects of Pentoxifylline: Profiling Data Based on RAW 264.7 Cellular Signaling

2021 ◽  
Vol 11 (17) ◽  
pp. 8273
Author(s):  
Mi Hyun Seo ◽  
Mi Young Eo ◽  
Truc Thi Hoang Nguyen ◽  
Hoon Joo Yang ◽  
Soung Min Kim
Keyword(s):  
High Performance ◽  
Expression Profiles ◽  
Severe Pneumonia ◽  
Cellular Level ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Cellular Apoptosis ◽  
Respiratory Tract Illness ◽  
Protein Expression Profiles ◽  
Related Proteins

Pentoxifylline (PTX) is a methylxanthine derivative that has been developed as an immunomodulatory agent and an improvement of microcirculation. Osteoradionecrosis (ORN) is a serious complication of radiation therapy due to hypovascularity. Coronavirus disease 2019 (COVID-19) has spread globally. Symptoms for this disease include self-limiting respiratory tract illness to severe pneumonia and acute respiratory distress. In this study, the effects of PTX on RAW 264.7 cells were investigated to reveal the possibility of PTX as a therapeutic agent for ORN and COVID-19. To reveal PTX effects at the cellular level, protein expression profiles were analyzed in the PTX-treated RAW 264.7 cells by using immunoprecipitation high-performance liquid chromatography (IP-HPLC). PTX-treated RAW 264.7 cells showed increases in immunity- and osteogenesis-related proteins and concurrent decreases in proliferation-, matrix inflammation-, and cellular apoptosis-related proteins expressions. The IP-HPLC results indicate that PTX plays immunomodulatory roles in RAW 264.7 cells by regulating anti-inflammation-, proliferation-, immunity-, apoptosis-, and osteogenesis-related proteins. These results suggest that PTX may be used as supplement medications for ORN as well as for COVID-19.

scholarly journals Expression of α-catenin in α-catenin–deficient cells increases resistance to sphingosine-induced apoptosis

2001 ◽  
Vol 154 (3) ◽  
pp. 573-584 ◽  
Author(s):  
Shyuichiro Matsubara ◽  
Masayuki Ozawa
Keyword(s):  
Cell Death ◽  
Cell Adhesion ◽  
Morphological Changes ◽  
Carcinoma Cells ◽  
Middle Segment ◽  
Cyclin Dependent Kinases ◽  
P27kip1 Protein ◽  
Colon Carcinoma Cells ◽  
Induced Apoptosis ◽  
Apoptotic Cascade

α-Catenin, an intracellular protein, associates with the COOH-terminal region of cadherin cell adhesion molecules through interactions with either β-catenin or γ-catenin (plakoglobin). The full activity of cadherins requires a linkage to the actin cytoskeleton mediated by catenins. We transfected α-catenin–deficient colon carcinoma cells with a series of α-catenin constructs to determine that α-catenin expression increases the resistance to apoptosis induced by sphingosine. Two groups of constructs, containing deletions in either the middle segment of the molecule or the COOH terminus, induced morphological changes, cell compaction, and decreases in cell death. In α-catenin–expressing cells, inhibition of cadherin cell adhesion by treatment with anti–E-cadherin antibodies did not decrease the cells viability. α-Catenin expression partially suppressed the downregulation of Bcl-xL and the activation of caspase 3. Expression of p27kip1 protein, an inhibitor of cyclin-dependent kinases, was increased by α-catenin expression in low density cell cultures. The increased levels of p27kip1 correlated with both increased resistance to cell death and morphological changes in transfectants containing deletion mutants. Transfection-mediated upregulation of p27kip1 decreases sphingosine-induced cell death in α-catenin–deficient cells. We postulate that α-catenin mediates transduction of signals from the cadherin–catenin complex to regulate the apoptotic cascade via p27kip1.

scholarly journals Farnesol-Induced Apoptosis in Candida albicans

2009 ◽  
Vol 53 (6) ◽  
pp. 2392-2401 ◽  
Author(s):  
Mark E. Shirtliff ◽  
Bastiaan P. Krom ◽  
Roelien A. M. Meijering ◽  
Brian M. Peters ◽  
Jingsong Zhu ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Protein Expression ◽  
Mammalian Cells ◽  
Expression Profiles ◽  
Fluorescent Microscopy ◽  
Physiological Role ◽  
Fungal Cell ◽  
Apoptotic Pathways ◽  
Induced Apoptosis ◽  
Protein Expression Profiles

ABSTRACT Farnesol, a precursor in the isoprenoid/sterol pathway, was recently identified as a quorum-sensing molecule produced by the fungal pathogen Candida albicans. Farnesol is involved in the inhibition of germination and biofilm formation by C. albicans and can be cytotoxic at certain concentrations. In addition, we have shown that farnesol can trigger apoptosis in mammalian cells via the classical apoptotic pathways. In order to elucidate the mechanism behind farnesol cytotoxicity in C. albicans, the response to farnesol was investigated, using proteomic analysis. Global protein expression profiles demonstrated significant changes in protein expression resulting from farnesol exposure. Among the downregulated proteins were those involved in metabolism, glycolysis, protein synthesis, and mitochondrial electron transport and the respiratory chain, whereas proteins involved in folding, protection against environmental and oxidative stress, actin cytoskeleton reorganization, and apoptosis were upregulated. Cellular changes that accompany apoptosis (regulated cell death) were further analyzed using fluorescent microscopy and gene expression analysis. The results indicated reactive oxygen species accumulation, mitochondrial degradation, and positive terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) in the farnesol-exposed cells concurrent with increased expression of antioxidant-encoding and drug response genes. More importantly, the results demonstrated farnesol-induced upregulation of the caspase gene MCA1 and the intracellular presence of activated caspases. In conclusion, this study demonstrated that farnesol promotes apoptosis in C. albicans through caspase activation, implying an important physiological role for farnesol in the fungal cell life cycle with important implications for adaptation and survival.

Isoliquiritigenin Inhibits Proliferation and Induces Apoptosis in Tongue Squamous Cell Carcinoma by Modulating miR-21/FOXG1 Pathway

2019 ◽  
Vol 17 (4) ◽  
pp. 463-469
Author(s):  
Hou Deqiang ◽  
Gao Yufeng ◽  
Bai Ning ◽  
Dong Yu
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Carcinoma Cells ◽  
Tongue Squamous Cell Carcinoma ◽  
Luciferase Assay ◽  
Forkhead Box ◽  
Proliferation And Apoptosis ◽  
Mrna And Protein Expression ◽  
Induced Apoptosis

Isoliquiritigenin is a flavonoid commonly found in liquorice and has been identified as a potent anti-tumor agent. The aim of this study was to investigate whether isoliquiritigenin regulates the proliferation and apoptosis of tongue squamous cell carcinoma cells by regulating forkhead box G1 expression via miR-21. MTT assay and flow cytometry were used to analyze cell proliferation and apoptosis, respectively. Quantitative real time polymerase chain reaction and western blotting were used to detect mRNA and protein expression levels, respectively. The relationship between miR-21 and forkhead box G1 was detected by dual luciferase assay. Isoliquiritigenin inhibited proliferation and induced apoptosis of tongue squamous cell carcinoma cells, and decreased miR-21 levels and promoted forkhead box G1 expression. Forkhead box G1 was then identified as a target of miR-21 and ISL could promote forkhead box G1 expression by inhibiting miR-21. Further analysis suggested that upregulation of miR-21 improved proliferation and suppressed apoptosis of tongue squamous cell carcinoma cells by inhibiting forkhead box G1 expression. Finally, our results revealed that isoliquiritigenin inhibited proliferation and induced apoptosis of tongue squamous cell carcinoma cells by regulating miR-21. Isoliquiritigenin might act as a novel therapeutic treatment for tongue squamous cell carcinoma cells through up-regulation of forkhead box G1 expression via inhibiting miR-21expression.

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