scholarly journals Antioxidant Peptide Derived fromSpirulina maximaSuppresses HIF1α-Induced Invasive Migration of HT1080 Fibrosarcoma Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-7
Author(s):  
Won Suk Kim ◽  
Won Kyo Jung ◽  
Sun Joo Park
Keyword(s):  
Cell Migration ◽  
Signaling Pathway ◽  
Ros Generation ◽  
Antioxidant Peptide ◽  
Intracellular Ros ◽  
Fibrosarcoma Cells ◽  
Ht1080 Cells ◽  
Human Fibrosarcoma Cells ◽  
Invasive Cell ◽  
Effective Cancer Therapy

Hypoxia causes the malignant progression of tumor cells; hence, it has been considered a central issue that must be addressed for effective cancer therapy. The initiation of tumor metastasis requires invasive cell migration. Here, we show that an antioxidant peptide derived fromSpirulina maximasuppresses hypoxia-induced invasive migration of HT1080 human fibrosarcoma cells. HT1080 cells treated with a hypoxia-inducing agent, CoCl2, exhibited an increase in invasive migration and intracellular reactive oxygen species (ROS), which is associated with an increase in the expression of hypoxia-induced factor 1α(HIF1α) accompanied by the activation of PI3K/Akt and ERK1/2. The inhibition of PI3K/Akt and ERK1/2 with specific inhibitors diminished the CoCl2-induced increase in HIF1αexpression and invasive cell migration. Moreover, CoCl2-induced HIF1αexpression was associated with an increase in the expression of molecules downstream ofβ-integrin, such as N-cadherin, vimentin, andβ-catenin. Therefore, theS. maximapeptide effectively attenuated the CoCl2-induced ROS generation and downregulated the HIF1αsignaling pathway involving PI3K/Akt, ERK1/2, andβ-integrin in cells. These results suggest that theS. maximaantioxidant peptide downregulates the HIF1αsignaling pathway necessary for hypoxia-induced invasive migration of HT1080 cells by attenuating intracellular ROS.S. maximapeptide may be an effective constituent in antitumor progression products.

Flavonoids Identified from Korean Scutellaria baicalensis Induce Apoptosis by ROS Generation and Caspase Activation on Human Fibrosarcoma Cells

2014 ◽  
Vol 42 (02) ◽  
pp. 465-483 ◽  
Author(s):  
Jue Zhang ◽  
Hyeon-Soo Park ◽  
Jin-A Kim ◽  
Gyeong-Eun Hong ◽  
ArulKumar Nagappan ◽  
...  
Keyword(s):  
Therapeutic Agent ◽  
Cancer Colorectal ◽  
Scutellaria Baicalensis ◽  
Ros Generation ◽  
Hnrnp K ◽  
Fibrosarcoma Cells ◽  
Ht1080 Cells ◽  
Cellular Pathways ◽  
Human Fibrosarcoma Cells ◽  
Induced Apoptosis

The effects of flavonoids from Korean Scutellaria baicalensis on fibrosarcoma HT1080 cells and their underlying molecular mechanism were investigated in this study. Flavonoids affected HT1080 cell proliferation by interrupting cell cycle progress, obviously augmenting the proportion of sub-G1 and diminishing that of G1 phase, and undergoing apoptosis at the tested dosage (100–400 μg/mL). In addition, the mediated apoptosis was mainly caused by total reactive oxygen species (ROS) generation and by up-regulating the ratio of Bax/Bcl-xL, triggering caspase cascades (caspase-3, -9 and -8), and inactivating PARP, dose-dependently. The proteomics results showed that AP-4, ARID 5B, HNRNP K, PLOG, Prdx6, and myosin-1, associated with cell growth, differentiation and development, and overexpressed in gastric cancer, colorectal cancer, pancreatic cancer, etc., were statistically down-regulated after the flavonoids treatment. Taken together, our data demonstrated that flavonoids from Korean S. baicalensis induced apoptosis in HT1080 cells, which involved a hierarchy of cellular pathways and multiple signal proteins, and might be a potential anticancer therapeutic agent.

scholarly journals TNP-470 Suppresses the Tumorigenicity of HT1080 Fibrosarcoma Tumor Through the Inhibition of VEGF Secretion From the Tumor Cells

Sarcoma ◽  
2001 ◽  
Vol 5 (4) ◽  
pp. 197-202 ◽  
Author(s):  
Mitsunori Kaya ◽  
Takuro Wada ◽  
Satoshi Nagoya ◽  
Satoshi Kawaguchi ◽  
Toshihiko Yamashita ◽  
...  
Keyword(s):  
Conditioned Medium ◽  
Direct Action ◽  
Angiogenesis Inhibitor ◽  
Angiogenesis Inhibitors ◽  
Fibrosarcoma Cells ◽  
Ht1080 Cells ◽  
Human Fibrosarcoma Cells ◽  
And Migration

Angiogenesis inhibitors are a novel class of promising therapeutic agents for treating cancer. TNP-470, a systemic analogue of fumagillin, is an angiogenesis inhibitor capable of suppressing the tumorigenicity in several animal models even though the mechanisms of action have not been completely clarified. In the current study, we investigated the effects of TNP-470 on human fibrosarcoma cellsin vivoandin vitro. The administration of TNP-470 could suppress the tumorigenicity of HT1080 fibrosarcoma tumor. The conditioned medium from HT1080 fibrosarcoma cells treated with TNP-470 inhibited the proliferation and migration of human endothelial cell line, HUVEC and ECV304. The concentration of VEGF in the conditioned medium from HT1080 cells treated with TNP-470 was lower than that of the cells without TNP-470 treatment, indicating that TNP-470 downregulates the secretion of VEGF from HT1080 cells. These findings strongly suggest that the direct action of TNP-470 on sarcoma cells inhibits angiogenesis through the downregulation of VEGF secretion and this angiogenesis suppression resulted in the inhibition of tumorigenicity of HT1080 fibrosarcoma tumo.

Adhesion dynamics and cytoskeletal structure of gliding human fibrosarcoma cells: a hypothetical model of cell migration

2003 ◽  
Vol 290 (2) ◽  
pp. 246-253 ◽  
Author(s):  
Sándor Paku ◽  
József Tóvári ◽  
Zsolt Lörincz ◽  
Ferenc Timár ◽  
Balázs Döme ◽  
...  
Keyword(s):  
Cell Migration ◽  
Hypothetical Model ◽  
Cytoskeletal Structure ◽  
Fibrosarcoma Cells ◽  
Human Fibrosarcoma Cells

scholarly journals Stanniocalcin 1 and 2 are secreted as phosphoproteins from human fibrosarcoma cells

2000 ◽  
Vol 350 (2) ◽  
pp. 453-461 ◽  
Author(s):  
Derek A. JELLINEK ◽  
Andy C. CHANG ◽  
Martin R. LARSEN ◽  
Xin WANG ◽  
Phillip J. ROBINSON ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Mammalian Cells ◽  
Phosphorylation Site ◽  
Mrna Levels ◽  
Intact Cells ◽  
Fibrosarcoma Cells ◽  
Ht1080 Cells ◽  
Human Fibrosarcoma Cells

Stanniocalcin 1 (STC1) and stanniocalcin 2 (STC2) are two recently identified mammalian peptide hormones. STC1 plays a role in calcium and phosphate homoeostasis, while the role of STC2 is unknown. We examined a human fibrosarcoma cell line, HT1080, that has high steady-state STC1 and STC2 mRNA levels, to determine whether these proteins are secreted. Following incubation of HT1080 cells with 32P, labelled STC1 and STC2 were found to be secreted into the medium. STC1 was phosphorylated in vitro by protein kinase C (PKC). In vitro and in vivo phosphorylation both occurred exclusively on serine and the phosphopeptide maps were similar, suggesting that PKC might be the in vivo kinase. STC2 was phosphorylated in vitro by casein kinase II (CK2), in vitro and in vivo phosphorylation were exclusively on serine and the phosphopeptide maps were indistinguishable. Phosphorylation of STC2 in intact cells resulted from the action of an ecto-protein kinase, since exogenous STC2 was phosphorylated by HT1080 cells and no phosphorylated STC2 was detectable inside the cells. The ectokinase activity was abolished by heparin and GTP could substitute for ATP as the phosphate donor, indicative of an ecto-CK2-like activity. The in vitro CK2 phosphorylation site was shown by matrix-assisted laser-desorption ionization–time-of-flight MS to be a single serine located between Ser-285 and Ser-298 in the C-terminal region of STC2. This is the first report of the secretion of STC1 or STC2 from mammalian cells. We conclude that these human fibrosarcoma cells express both STC1 and STC2 as secreted phosphoproteins in vivo, with STC2 being phosphorylated by an ecto-CK2-like enzyme.

scholarly journals Activation of PAR-1/NADPH Oxidase/ROS Signaling Pathways is Crucial for the Thrombin-Induced sFlt-1 Production in Extravillous Trophoblasts: Possible Involvement in the Pathogenesis of Preeclampsia

2015 ◽  
Vol 35 (4) ◽  
pp. 1654-1662 ◽  
Author(s):  
Qi-tao Huang ◽  
Jian-hong Chen ◽  
Li-lin Hang ◽  
Shi-san Liu ◽  
Mei Zhong
Keyword(s):  
Nadph Oxidase ◽  
Signaling Pathway ◽  
First Trimester ◽  
Ros Generation ◽  
Dependent Manner ◽  
Ros Signaling ◽  
Protein Levels ◽  
Intracellular Ros ◽  
Interfering Rna ◽  
Extravillous Trophoblasts

Backgrounds/Aims: Preeclampsia was characterized by excessive thrombin generation in placentas and previous researches showed that thrombin could enhance soluble Fms-like tyrosine kinase 1 (sFlt-1) expression in first trimester trophoblasts. However, the detailed mechanism for the sFlt-1 over-production induced by thrombin was largely unknown. The purpose of this study was to explore the possible signaling pathway of thrombin-induced sFlt-1 production in extravillous trophoblasts (EVT). Methods: An EVT cell line (HRT-8/SVneo) was treated with various concentrations of thrombin. The mRNA expression and protein secretion of sFlt-1 in EVT were detected with real-time polymerase chain reaction and ELISA, respectively. The levels of intracellular reactive oxygen species (ROS) production were determined by DCFH-DA. Results: Exposure of EVT to thrombin induced increased intracellular ROS generation and overexpression of sFlt-1 at both mRNA and protein levels in a dose dependent manner. Short interfering RNA (siRNA) directed against PAR-1 or apocynin (an inhibitor of NADPH oxidase) could decrease the intracellular ROS generation and subsequently suppressed the production of sFlt-1 at mRNA and protein levels. Conclusions: Our results suggested that thrombin increased sFlt-1 production in EVT via the PAR-1 /NADPH oxidase /ROS signaling pathway. This also highlights the PAR-1 / NADPH oxidase / ROS pathway might be a potential therapeutic target for the prevention of preeclampsia in the future.

Quercetin Suppresses Intracellular ROS Formation, MMP Activation, and Cell Motility in Human Fibrosarcoma Cells

2013 ◽  
Vol 78 (9) ◽  
pp. H1464-H1469 ◽  
Author(s):  
Dong Eun Lee ◽  
Min-Yu Chung ◽  
Tae Gyu Lim ◽  
Won Bum Huh ◽  
Hyong Joo Lee ◽  
...  
Keyword(s):  
Cell Motility ◽  
Intracellular Ros ◽  
Fibrosarcoma Cells ◽  
Ros Formation ◽  
Human Fibrosarcoma Cells
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