Search results for "Cancer cell"

CYTOTOXIC POTENTIAL OF AQUEOUS EXTRACTS FROM RHIZOMES AND LEAVES OF POSIDONIA OCEANICA (L.) DELILE AGAINST HEPG2 CANCER CELLS

2022

Gene and protein signatures associated to treatment of MDA-MB231 breast cancer cells with JAHA, a novel histone deacetylase inhibitor

2014

The effect of the HDACi JAHA on DNA methylation of breast cancer cells by down-regulating DNMT1 through ERK signaling

2014

Evaluation of the in vitro and in vivo antineoplastic effects of Parthenolide on MDA-MB231 breast cancer cells

2012

Triple-negative breast cancer refers to an aggressive subtype of breast cancer in which the tumor cells lack receptors for estrogen, progesterone and the HER2 protein on their surfaces. This type of breast cancer does not respond to treatments such as hormone therapy, like tamoxifen and aromatase inhibitors, or drugs that target HER2, like Herceptin. It is important, therefore, the identification of new selective drugs for the treatment of these tumors. Parthenolide (PN), a sesquiterpene lactone extracted from the medical plant Tanacetum parthenium, exerts anticancer activity on several tumor cell lines in culture, acting through diverse molecular mechanisms. Our previous studies have shown…

The mechanism by which histone deacetylase inhibitors sensitize hepatoma and colon cancer cells to TRAIL-induced apoptosis

2008

PROTEOMIC ANALYSIS OF VESICLES SHED BY BREAST CANCER CELLS IN VITRO

2011

Expression of angiogenic regulators. VEGF and leptin, is regulated by the EGF/P13K/STAT3 pathway in colorectal cancer cells

2009

Cancer cell(s) cycle sequencing reveals universal mechanisms of apoptosis

2010

In this paper, cell cycle in higher eukaryotes and their molecular networks signals both in G 1/S and G2/M transitions are replicated in silico. Biochemical kinetics, converted into a set of differential equations, and system control theory are employed to design multi-nested digital layers to simulate protein-to-protein activation and inhibition for cell cycle dynamics in the presence of damaged genomes. Sequencing and controlling the digital process of four micro-scale species networks (p53/Mdm2/DNA damage, p21mRNA/cyclin-CDK complex, CDK/CDC25/wee1/ SKP2/APC/CKI and apoptosis target genes system) not only allows the comprehension of the mechanisms of these molecule interactions but paves…

On p21 tracking property in cancer cell unravelled bio-digitally in silico. Are apoptosis principles universal?

2010

Upon severe DNA damage, p21 acts in a dual mode; on the one hand, it inhibits the cyclin-CDK complex for arresting the G2/M transition and on the other hand, it indirectly becomes an apoptotic factor by activating--in sequence--the retinoblastoma protein, E2F1 and APAF1 expressions. But, in a cancer cells proliferation, the mechanisms of, and participants in, the apoptosis failure remain unclear. Since the p21/p53/Mdm2 proteins network normally involves a digital response in a cancer cell, through an original design of a cell signalling-protein simulator, we demonstrate, in silico, that apoptosis phase instability is fully reciprocated by p21 mRNA irregular dynamics which operates according…

Combining conventional chemotherapy and γδ T cell-based immunotherapy to target cancer-initiating cells.

2013

Colon cancer comprises a small population of cancer initiating stem cells (CIC) that is responsible for tumor maintenance and resistance to anti-cancer therapies, possibly allowing for tumor recapitulation once treatment stops. Combinations of immune-based therapies with chemotherapy and other anti-tumor agents may be of significant clinical benefit in the treatment of colon cancer. However, cellular immune-based therapies have not been experimented yet in the population of colon CICs. Here, we demonstrate that treatment with low concentrations of commonly used chemotherapeutic agents, 5-fluorouracyl and doxorubicin, sensitize colon CICs to Vγ9Vδ2 T cell cytotoxicity. Vγ9Vδ2 T cell cytotoxi…