scholarly journals Vitamin K enhancement of sorafenib-mediated HCC cell growth inhibition in vitro and in vivo

2010 ◽  
Vol 127 (12) ◽  
pp. 2949-2958 ◽  
Author(s):  
Gang Wei ◽  
Meifang Wang ◽  
Terry Hyslop ◽  
Ziqiu Wang ◽  
Brian I. Carr
Keyword(s):  
Cell Growth ◽  
Growth Inhibition ◽  
Vitamin K ◽  
Cell Growth Inhibition

Anti-cancer effect of adenovirus p53 on human cervical cancer cell growth in vitro and in vivo

2004 ◽  
Vol 14 (2) ◽  
pp. 322-332 ◽  
Author(s):  
W. S. Ahn ◽  
S. M. Bae ◽  
J. M. Lee ◽  
S. E. Namkoong ◽  
J. Y. Yoo ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Cancer Cell ◽  
Cervical Cancer Cell ◽  
Transduction Efficiency ◽  
Cell Growth Inhibition ◽  
P53 Expression

To evaluate anti-tumor effects of recombinant adenovirus p53, time-course p53, E6 expression, and cell growth inhibition were investigated in vitro and in vivo using cervical cancer cell lines such as CaSki, SiHa, HeLa, HeLaS3, C33A, and HT3. The cell growth inhibition was studied via cell count assay, MTT assay and neutral red assay. After transfecting AdCMVp53 into SiHa cells-xenografted nude mice, the transduction efficiency and anti-tumor effect were investigated for a month. The results showed that adenoviral p53 expression induced significant growth suppression on the cancer cells, in which E6 transcript was strongly repressed, and that the expression of p53 and E6 were remarkably dependent on each cell type. The transduction efficiency was highly maintained in vivo as well as in vitro, and the size of tumor was remarkably decreased in comparison with AdCMVLacZ control. The results suggest that the adenovirus-mediated p53 gene transfection was done very effectively in vitro and in vivo experiment, and the cell growth was suppressed via p53-dependent apoptotic cell death, and that the anti-tumor effect could be related to E6 and p53 expression pattern.

A novel zinc-chelating small molecule exhibits cancer cell growth inhibition in vitro and in vivo by induction of tumor suppressors early growth response 1 (Egr-1) and Krüppel-Like Factor 4 (KLF4)

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 14084-14084
Author(s):  
L. Lock ◽  
A. Khine ◽  
M. Huesca ◽  
V. Lawson ◽  
R. Peralta ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Cancer Cell ◽  
Phase Cell ◽  
Cell Growth Inhibition ◽  
Ht 29

14084 Background: Lead compound LT-253 was selected from a group of 2-indolyl imidazol [4,5-d] phenanthroline derivatives with anticancer activity. It shows potent and selective anti-proliferative activity against several human cancer types in vitro, and in vivo in xenograft mouse models of human colon carcinoma (HT-29) and non-small cell lung carcinoma (H460). Methods: The mechanism of cell growth inhibition of LT-253 was investigated in HT-29 colon cancer cells using the XTT cell proliferation assay, flow cytometry and apoptosis assays. In vitro and in vivo zinc chelation was determined by competition assays using fluorescent and chromophoric chelators. Gene expression studies were performed by human genome microarray analysis and confirmed by quantitative real- time PCR. The transcription factor activity profile of LT-253-treated cells was determined by a multiplex transcription factor array and electrophoretic mobility shift assays. The functional role of specific genes was evaluated by siRNA gene knock-down. Results: LT-253 functions as chelator of zinc in vitro, and of intracellular labile zinc in HT-29 cells. Moreover, LT-253-mediated HT-29 cell growth inhibition was reversed by zinc supplementation. Gene expression profiling confirmed sustained changes in zinc-sensitive genes such as metallothionine and several zinc transporters, but not copper-sensitive or iron-sensitive genes. LT-253 induces cancer cell growth inhibition primarily through G1/S phase cell cycle arrest. Gene expression and transcription factor activities of both Egr-1 and KLF4 are induced within 4 hr post LT-253 treatment. Moreover, increased expression of both Egr-1 and KLF4 is observed in LT-253-sensitive cancer cell lines of various origins. Importantly, Egr-1 and KLF4 gene knock-down by siRNA reversed the LT-253-mediated cell growth inhibition of HT-29 cells. Conclusion: Selective chelation of intracellular labile zinc pool by LT-253 triggers immediate induction of stress-responsive tumor suppressor Egr-1 and sustained induction of zinc-responsive tumor suppressor KLF4, leading to G1/S phase cell cycle arrest and inhibition of tumor growth. No significant financial relationships to disclose.

In vitro and in vivo Study of Cell Growth Inhibition of Simvastatin on Chronic Myelogenous Leukemia Cells

Chemotherapy ◽  
2008 ◽  
Vol 54 (6) ◽  
pp. 438-446 ◽  
Author(s):  
Yong-Chang Yang ◽  
Wen-Fang Huang ◽  
Liang-Min Chuan ◽  
Dai-Wen Xiao ◽  
Ya-Li Zeng ◽  
...  
Keyword(s):  
Cell Growth ◽  
Growth Inhibition ◽  
Chronic Myelogenous Leukemia ◽  
Myelogenous Leukemia ◽  
In Vivo Study ◽  
Leukemia Cells ◽  
Cell Growth Inhibition ◽  
Chronic Myelogenous Leukemia Cells

scholarly journals New In Vitro-In Silico Approach for the Prediction of In Vivo Performance of Drug Combinations

Molecules ◽  
2021 ◽  
Vol 26 (14) ◽  
pp. 4257
Author(s):  
Cristiana Correia ◽  
Abigail Ferreira ◽  
Joana Santos ◽  
Rui Lapa ◽  
Marjo Yliperttula ◽  
...  
Keyword(s):  
Cell Growth ◽  
Growth Inhibition ◽  
In Silico ◽  
Single Agent ◽  
Drug Combinations ◽  
In Vitro Assays ◽  
Cell Growth Inhibition ◽  
Time Curve

Pharmacokinetic (PK) studies improve the design of dosing regimens in preclinical and clinical settings. In complex diseases like cancer, single-agent approaches are often insufficient for an effective treatment, and drug combination therapies can be implemented. In this work, in silico PK models were developed based on in vitro assays results, with the goal of predicting the in vivo performance of drug combinations in the context of cancer therapy. Combinations of reference drugs for cancer treatment, gemcitabine and 5-fluorouracil (5-FU), and repurposed drugs itraconazole, verapamil or tacrine, were evaluated in vitro. Then, two-compartment PK models were developed based on the previous in vitro studies and on the PK profile reported in the literature for human patients. Considering the quantification parameter area under the dose-response-time curve (AUCeffect) for the combinations effect, itraconazole was the most effective in combination with either reference anticancer drugs. In addition, cell growth inhibition was itraconazole-dose dependent and an increase in effect was predicted if itraconazole administration was continued (24-h dosing interval). This work demonstrates that in silico methods and AUCeffect are powerful tools to study relationships between tissue drug concentration and the percentage of cell growth inhibition over time.

scholarly journals Effect of β-carotene-rich tomato lycopene β-cyclase (tlcy-b) on cell growth inhibition in HT-29 colon adenocarcinoma cells

2008 ◽  
Vol 102 (2) ◽  
pp. 207-214 ◽  
Author(s):  
Paola Palozza ◽  
Diana Bellovino ◽  
Rossella Simone ◽  
Alma Boninsegna ◽  
Francesco Cellini ◽  
...  
Keyword(s):  
Cell Growth ◽  
Growth Inhibition ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Cell Growth Inhibition ◽  
Adenocarcinoma Cells ◽  
Ht 29 ◽  
Colon Adenocarcinoma Cells ◽  
Β Carotene

Lycopene β-cyclase (tlcy-b) tomatoes, obtained by modulating carotenogenesis via genetic engineering, contain a large amount of β-carotene, as clearly visible by their intense orange colour. In the present study we have subjected tlcy-b tomatoes to an in vitro simulated digestion and analysed the effects of digestate on cell proliferation. To this aim we used HT-29 human colon adenocarcinoma cells, grown in monolayers, as a model. Digested tomatoes were diluted (20 ml, 50 ml and 100 ml/l) in culture medium and added to the cells for different incubation times (24 h, 48 h and 72 h). Inhibition of cell growth by tomato digestate was dose-dependent and resulted from an arrest of cell cycle progression at the G0/G1 and G2/M phase and by apoptosis induction. A down-regulation of cyclin D1, Bcl-2 and Bcl-xl expression was observed. We also found that heat treatment of samples before digestion enhanced β-carotene release and therefore cell growth inhibition. To induce with purified β-carotene solubilised in tetrahydrofuran the same cell growth inhibition obtained with the tomato digestate, a higher amount of the carotenoid was necessary, suggesting that β-carotene micellarised during digestion is utilised more efficiently by the cells, but also that other tomato molecules, reasonably made available during digestion, may be present and cooperate with β-carotene in promoting cell growth arrest.

A Facile Synthesis of 9-Deaza Analogue of Olomoucine

2003 ◽  
Vol 68 (4) ◽  
pp. 779-791 ◽  
Author(s):  
Petr Čapek ◽  
Miroslav Otmar ◽  
Milena Masojídková ◽  
Ivan Votruba ◽  
Antonín Holý
Keyword(s):  
Cell Growth ◽  
Growth Inhibition ◽  
Cell Lines ◽  
Alkaline Solution ◽  
Catalytic Hydrogenation ◽  
Cell Growth Inhibition ◽  
Facile Synthesis ◽  
Hydroxymethyl Group ◽  
Chloro Derivative

Heating of 6-(benzylamino)-2-chloro-9-deazapurine (3) with ethanolamine afforded 6-(benzylamino)-2-[(2-hydroxyethyl)amino]-9-deazapurine (8). Its treatment with formaldehyde in alkaline solution, after protection of the OH group with DMTr, led to hydroxymethylation at position 9. Conversion of the hydroxymethyl group to methyl was performed by catalytic hydrogenation under simultaneous deprotection, which resulted in the formation of the 9-deaza analogue 1 of olomoucine. Compound 1 does not exhibit any significant in vitro cell growth inhibition of CCRF-CEM, HeLa and L-1210 cell lines. Cytostatic activity was found in 6-(benzylamino)-9-deazapurine (2) and its 2-chloro derivative 3 in CCRF-CEM cells with IC50 13.3 and 15.8 μM, respectively.

Novel domain-targeted anti-Trop-2 monoclonal antibodies to elicit therapeutic synergy against multiple human cancers.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e14002-e14002
Author(s):  
Saverio Alberti ◽  
Marco Trerotola ◽  
Valeria Relli ◽  
Chiara Pedicone ◽  
Antonella D' Amore ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Transmembrane Domain ◽  
Human Cancer ◽  
Expression System ◽  
Calcium Signal ◽  
Globular Domain

e14002 Background: Trop-2 is a calcium signal transducer that drives tumor cell growth. Trop-2 is overexpressed in the majority of carcinomas, where it associates with worse prognosis. The Trop-2 extracellular domain contains a N-terminal cysteine-rich globular domain followed by a stem-like cysteine-less region that connects to the transmembrane domain. Trop-2 engages in homophylic interactions between adjacent cells and interacts with tight-junction proteins, which may severely affect accessibility by therapeutic monoclonal antibodies (mAb). Available anti-Trop-2 mAb mostly recognize a single immunodominant epitope between the globular and stem regions, and have limited or no therapeutic efficacy. In order to untap the potential of anti-Trop-2 immunotherapy we generated novel anti-Trop-2 mAb with tailored specificity towards the globular versus stem regions. Methods: Balb-C mice were immunized with soluble human Trop-2 produced in human 293 and murine L cell lines and in baculovirus expression system. Domain-targeted anti-Trop-2 mAb were selected by flow cytometry using live 293 transfectants.Therapeutic potential was assessed in human cancer xenografts in murine models. mAb mode of action was investigated by Western blot, live-cell imaging and in vitro ADCC and cancer cell growth inhibition assays. Results: mAb were identified that were differentially directed against the Trop-2 stem versus globular regions. These mAb efficiently bound Trop-2 expressing cancer cells and inhibited cell growth in vitro. In vivo, naked anti-globular OX-G64 and anti-stem OX-S55 mAb were most effective in inhibiting the growth of colon, ovary, breast and prostate cancers as xenografts in nude mice. NSG mice and in vitro mechanism profiling indicated efficient ADCC, together with efficient internalization for ADC development. Differential efficacy for established tumors versus isolated-cell models of metastatic dissemination was shown. Most remarkably, OX-G64/OX-S55 co-administration demonstrated sinergic growth inhibition in vivo. Conclusions: The OX-G64 and OX-S55 anti-Trop-2 mAb are novel domain-targeted, sinergic therapeutic mAb for game-changing anti-cancer immunotherapy.

scholarly journals Mechanism of In vitro Pancreatic Cancer Cell Growth Inhibition by Melanoma Differentiation–Associated Gene-7/Interleukin-24 and Perillyl Alcohol

2008 ◽  
Vol 68 (18) ◽  
pp. 7439-7447 ◽  
Author(s):  
Irina V. Lebedeva ◽  
Zhao-zhong Su ◽  
Nichollaq Vozhilla ◽  
Lejuan Chatman ◽  
Devanand Sarkar ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Perillyl Alcohol ◽  
Cell Growth Inhibition ◽  
Cancer Cell Growth
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