Vitronetcin promotes cell growth and inhibits apoptotic stimuli in a human hepatoma cell line via the activation of caspases

2014 ◽  
Vol 92 (5) ◽  
pp. 363-368 ◽  
Author(s):  
Wei Zhu ◽  
Yingzhi Liu ◽  
Konghe Hu ◽  
Wenxue Li ◽  
Jianling Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Tumor Cell ◽  
Hepatoma Cell ◽  
Hepatoma Cells ◽  
Signaling Molecules ◽  
Hepatoma Cell Line ◽  
Dependent Manner ◽  
Tumor Cell Growth ◽  
Induced Apoptosis

This study sought to understand the effects of vitronectin (VTN) on the growth of SMMC-7721 hepatoma cells. In addition, this study examined how VTN inhibits the induction of apoptosis in SMMC-7721 cells by 3,3′-diindolylmethane (DIM), a metabolite of natural phytochemicals, and preliminarily investigated the signaling molecules involved in this process. A cell proliferation reagent was used to observe the effects of VTN on cell proliferation rates. Laser scanning confocal microscopy was performed to observe the effects of VTN on the morphology of tubulin, a component of the cytoskeleton. Flow cytometry and Western blotting assays were used to observe the inhibitory effects of VTN on DIM-induced apoptosis in SMMC-7721 cells and changes in the expression levels of the signaling molecules involved in this process. VTN promoted tumor cell growth in a concentration-dependent manner and inhibited apoptosis caused by the effects of apoptosis-inducing agents. Under in vitro experimental conditions, VTN contributed to the growth of SMMC-7721 hepatoma cells and protected them from the effects of an apoptosis-inducing agent. These findings suggest that during hepatocellular carcinogenesis, VTN may promote tumor cell growth and inhibit chemically induced apoptosis.

Inhibitory Effects of Lycopene on the Adhesion, Invasion, and Migration of SK-Hep1 Human Hepatoma Cells

2006 ◽  
Vol 231 (3) ◽  
pp. 322-327 ◽  
Author(s):  
Eun-Sun Hwang ◽  
Hyong Joo Lee
Keyword(s):  
Cell Growth ◽  
Hepatoma Cell ◽  
Hepatoma Cells ◽  
Hepatoma Cell Line ◽  
Dependent Manner ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Human Hepatoma Cell ◽  
Invasion And Migration ◽  
And Migration

Lycopene, which is the predominant carotenoid in tomatoes and tomato-based foods, may protect humans against various cancers. Effects of lycopene on the adhesion, invasion, migration, and growth of the SK-Hep1 human hepatoma cell line were investigated. Lycopene inhibited cell growth in dose-dependent manners, with growth inhibition rates of 5% and 40% at 0.1 μM and 50 μM lycopene, respectively, after 24 hrs of incubation. Similarly, after 48 hrs of incubation, lycopene at 5 μM and 10 μM decreased the cell numbers by 30% and 40%, respectively. Lycopene decreased the gelatinolytic activities of both matrix metalloproteinase (MMP)-2 and MMP-9, which were secreted from the SK-Hep1 cells. Incubation of SK-Hep1 cells with 110 μM of lycopene for 60 mins significantly inhibited cell adhesion to the Matrigel-coated substrate in a concentration-dependent manner. To study invasion, SK-Hep1 cells were grown either on Matrigel-coated Transwell membranes or in 24-well plates. The cells were treated sequentially for 24 hrs with lycopene before the start of the invasion assays. Cell growth and death were assessed under the same conditions. The invasion of SK-Hep1 cells treated with lycopene was significantly reduced to 28.3% and 61.9% of the control levels at 5 μM and 10 μM lycopene, respectively (P < 0.05). In the migration assay, lycopene-treated cells showed lower levels of migration than untreated cells. These results demonstrate the antimetastatic properties of lycopene in inhibiting the adhesion, invasion, and migration of SK-Hep1 human hepatoma cells.

scholarly journals p120 catenin induces opposing effects on tumor cell growth depending on E-cadherin expression

2008 ◽  
Vol 183 (4) ◽  
pp. 737-749 ◽  
Author(s):  
Edwin Soto ◽  
Masahiro Yanagisawa ◽  
Laura A. Marlow ◽  
John A. Copland ◽  
Edith A. Perez ◽  
...  
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Mitogen Activated Protein Kinase ◽  
Dependent Manner ◽  
Tumor Cell Growth ◽  
P120 Catenin ◽  
Opposing Effects ◽  
E Cadherin

p120 catenin regulates the activity of the Rho family guanosine triphosphatases (including RhoA and Rac1) in an adhesion-dependent manner. Through this action, p120 promotes a sessile cellular phenotype when associated with epithelial cadherin (E-cadherin) or a motile phenotype when associated with mesenchymal cadherins. In this study, we show that p120 also exerts significant and diametrically opposing effects on tumor cell growth depending on E-cadherin expression. Endogenous p120 acts to stabilize E-cadherin complexes and to actively promote the tumor-suppressive function of E-cadherin, potently inhibiting Ras activation. Upon E-cadherin loss during tumor progression, the negative regulation of Ras is relieved; under these conditions, endogenous p120 promotes transformed cell growth both in vitro and in vivo by activating a Rac1–mitogen-activated protein kinase signaling pathway normally activated by the adhesion of cells to the extracellular matrix. These data indicate that both E-cadherin and p120 are important regulators of tumor cell growth and imply roles for both proteins in chemoresistance and targeted therapeutics.

Abstract 1227: New small molecules targeting MYC:MAX interactions that inhibits tumor cell growth in a MYC-dependent manner

2016 ◽  
Author(s):  
Alina Castell ◽  
Karin Ridderstråle ◽  
Qinzi Yan ◽  
Fan Zhang ◽  
Per Hydbring ◽  
...  
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Small Molecules ◽  
Dependent Manner ◽  
Tumor Cell Growth

Inhibition of tumor angiogenesis in vivo by a monoclonal antibody targeted to domain 5 of high molecular weight kininogen

Blood ◽  
2004 ◽  
Vol 104 (7) ◽  
pp. 2065-2072 ◽  
Author(s):  
James S. Song ◽  
Irma M. Sainz ◽  
Stephen C. Cosenza ◽  
Irma Isordia-Salas ◽  
Abdel Bior ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Monoclonal Antibody ◽  
Cell Growth ◽  
Tumor Cell ◽  
High Molecular Weight ◽  
Control Group ◽  
Dependent Manner ◽  
Tumor Cell Growth ◽  
High Molecular Weight Kininogen

Abstract We have shown that human high molecular weight kininogen is proangiogenic due to release of bradykinin. We now determined the ability of a murine monoclonal antibody to the light chain of high molecular weight kininogen, C11C1, to inhibit tumor growth compared to isotype-matched murine IgG. Monoclonal antibody C11C1 efficiently blocks binding of high molecular weight kininogen to endothelial cells in a concentration-dependent manner. The antibody significantly inhibited growth of human colon carcinoma cells in a nude mouse xenograft assay and was accompanied by a significant reduction in the mean microvascular density compared to the IgG control group. We also showed that a hybridoma producing monoclonal antibody C11C1 injected intramuscularly exhibited markedly smaller tumor mass in a syngeneic host compared to a hybridoma producing a monoclonal antibody to the high molecular weight kininogen heavy chain or to an unrelated plasma protein. In addition, tumor inhibition by purified monoclonal antibody C11C1 was not due to direct antitumor effect because there was no decrease of tumor cell growth in vitro in contrast to the in vivo inhibition. Our results indicate that monoclonal antibody C11C1 inhibits angiogenesis and human tumor cell growth in vivo and has therapeutic potential for treatment of human cancer. (Blood. 2004;104:2065-2072)

scholarly journals Co-culture of hepatoma cells with hepatocytic precursor (stem-like) cells inhibits tumor cell growth and invasion by downregulating Akt/NF-κB expression

2016 ◽  
Vol 12 (5) ◽  
pp. 4054-4060
Author(s):  
Cheng-Jun Sui ◽  
Miao Xu ◽  
Wei-Qing Li ◽  
Jia-Mei Yang ◽  
Hong-Zhu Yan ◽  
...  
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Hepatoma Cells ◽  
Tumor Cell Growth

In situ condensation of an anti-cancer drug into fibrin gel enabling effective inhibition of tumor cell growth

2019 ◽  
Vol 55 (78) ◽  
pp. 11679-11682 ◽  
Author(s):  
Masayasu Kuwahara ◽  
Hiroto Fujita ◽  
Yuka Kataoka ◽  
Yasuyo Nakajima ◽  
Masanobu Yamada ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Tumor Cell ◽  
Cancer Drug ◽  
Tumor Cell Growth ◽  
Fibrin Gel ◽  
Anti Cancer ◽  
Effective Inhibition

Efficient anti-cancer drug condensation enabled equally inhibiting cell proliferation even at a concentration of 7.6 ± 0.36 nM, which was approximately 170-fold lower than the standard therapeutic concentrations of camptothecin (CPT) drugs.

scholarly journals Trichinella spiralis ESP inhibits tumor cell growth by regulating the immune response and inducing apoptosis

2021 ◽  
Author(s):  
Jing Ding ◽  
Xiaolei Liu ◽  
Bin Tang ◽  
Xue Bai ◽  
Yang Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Tumor Cell ◽  
Trichinella Spiralis ◽  
Tumor Model ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Secretory Product ◽  
Tumor Cell Growth ◽  
Th1 Cytokines

Abstract Background Although Trichinella spiralis (T. spiralis) causes zoonotic diseases, it has a strong immunomodulatory effect and has therapeutic potential for various autoimmune diseases and cancers. Our previous study results showed that T. spiralis infection can inhibit the growth of liver cancer cells, but the specific mechanism has not been elucidated. Methods BALB/c mice injected with H22 cells and then infected with T. spiralis were used to detect tumor inhibition rate. Cell proliferation and apoptosis of H22 cells treated with excretory-secretory product (ESP) were measured by Cell-Counting Kit 8 (CCK-8) and Flow Cytometry (FCM). The expression of apoptosis-related genes in H22 cells and tumor tissues was detected by western blotting and real-time quantitative PCR (qPCR). IL-2, IFN-γ and IL-4 production in the spleens were measured by qPCR and enzyme-linked immunosorbent assay(ELISA). Results The growth of tumors in tumor model mice infected with T. spiralis was significantly inhibited compared with those uninfected tumor model mice. ESP could inhibit H22 cell proliferation and induce apoptosis through the mitochondrial pathway both in vitro and in vivo. Additionally, the levels of Th1 cytokines with antitumor effects were significantly increased in the early stage of T. spiralis infection, while Th2 cytokines increased later than Th1 cytokines. Conclusions ESP can directly induce tumor cell apoptosis and indirectly inhibit tumor cell growth through the host immune system, which is the potential antitumor mechanism of T. spiralis infection.

Effects of Selaginella tamariscina on in vitro tumor cell growth, p53 expression, G1 arrest and in vivo gastric cell proliferation

1999 ◽  
Vol 144 (1) ◽  
pp. 93-99 ◽  
Author(s):  
In-Seon Lee ◽  
Akiyoshi Nishikawa ◽  
Fumio Furukawa ◽  
Ken-ichiro Kasahara ◽  
Soo-Un Kim
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Tumor Cell ◽  
G1 Arrest ◽  
Tumor Cell Growth ◽  
P53 Expression ◽  
Gastric Cell ◽  
Selaginella Tamariscina

scholarly journals Shikonin Reduces Growth of Docetaxel-Resistant Prostate Cancer Cells Mainly through Necroptosis

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 882
Author(s):  
Sascha D. Markowitsch ◽  
Kira M. Juetter ◽  
Patricia Schupp ◽  
Kristine Hauschulte ◽  
Olesya Vakhrusheva ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Tumor Cell ◽  
Metabolic Activity ◽  
Treatment Options ◽  
Therapy Resistance ◽  
Tumor Cell Growth ◽  
Antitumor Effects ◽  
New Treatment ◽  
Induced Apoptosis

The prognosis for advanced prostate carcinoma (PCa) remains poor due to development of therapy resistance, and new treatment options are needed. Shikonin (SHI) from Traditional Chinese Medicine has induced antitumor effects in diverse tumor entities, but data related to PCa are scarce. Therefore, the parental (=sensitive) and docetaxel (DX)-resistant PCa cell lines, PC3, DU145, LNCaP, and 22Rv1 were exposed to SHI [0.1–1.5 μM], and tumor cell growth, proliferation, cell cycling, cell death (apoptosis, necrosis, and necroptosis), and metabolic activity were evaluated. Correspondingly, the expression of regulating proteins was assessed. Exposure to SHI time- and dose-dependently inhibited tumor cell growth and proliferation in parental and DX-resistant PCa cells, accompanied by cell cycle arrest in the G2/M or S phase and modulation of cell cycle regulating proteins. SHI induced apoptosis and more dominantly necroptosis in both parental and DX-resistant PCa cells. This was shown by enhanced pRIP1 and pRIP3 expression and returned growth if applying the necroptosis inhibitor necrostatin-1. No SHI-induced alteration in metabolic activity of the PCa cells was detected. The significant antitumor effects induced by SHI to parental and DX-resistant PCa cells make the addition of SHI to standard therapy a promising treatment strategy for patients with advanced PCa.

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