scholarly journals The Impact of Cetuximab Plus AKT- or mTOR- Inhibitor in a Patient-Derived Colon Cancer Cell Model with Wild-Type RAS and PIK3CA Mutation

2017 ◽  
Vol 8 (14) ◽  
pp. 2713-2719 ◽  
Author(s):  
Ju Sun Kim ◽  
Jung Eun Kim ◽  
Kyung Kim ◽  
Jeeyun Lee ◽  
Joon Oh Park ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cell ◽  
Mtor Inhibitor ◽  
Cell Model ◽  
Pik3ca Mutation ◽  
Colon Cancer Cell ◽  
Wild Type ◽  
The Impact

The impact of cetuximab plus AKT- or mTOR- inhibitor in patient-derived colon cancer cell model with RAS wild type and PIK3CA mutation.

2016 ◽  
Vol 34 (15_suppl) ◽  
pp. e15153-e15153
Author(s):  
Seung Tae Kim ◽  
Su Jin Lee ◽  
Joon Oh Park ◽  
Ho Yeong Lim ◽  
Won Ki Kang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cell ◽  
Mtor Inhibitor ◽  
Cell Model ◽  
Pik3ca Mutation ◽  
Colon Cancer Cell ◽  
Wild Type ◽  
The Impact

The impact of pyrvinium pamoate on colon cancer cell viability

2014 ◽  
Vol 29 (10) ◽  
pp. 1189-1198 ◽  
Author(s):  
Armin Wiegering ◽  
Friedrich-Wilhelm Uthe ◽  
Melanie Hüttenrauch ◽  
Bettina Mühling ◽  
Michael Linnebacher ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Viability ◽  
Cancer Cell ◽  
Colon Cancer Cell ◽  
The Impact ◽  
Pyrvinium Pamoate

scholarly journals hCAIX Expression and Cell Cycle in Cytokine Stimulated Human Colon Cancer Cells

2019 ◽  
Author(s):  
Rahsan Ilikci Sagkan ◽  
Feray Kockar ◽  
Ali Sengul ◽  
Sukran Yilmaz ◽  
Ugur Musabak
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Colon Carcinoma ◽  
Cancer Cell ◽  
Cell Model ◽  
Hot Spot ◽  
Colon Cancer Cell ◽  
Expression Level ◽  
Colon Cells ◽  
Ht 29

Abstract Background: At the aim of this study, we investigated the effects of different kind of cytokines and the combinations of which on human carbonic anhydrase IX ( hCAIX) expression in HT-29 cell selected as colon carcinoma model for different doses and time of exposure to determine role of cytokines for treatment of colon carcinoma cells. Results: To sum up, h CA9 expression in the levels of gene and protein increased in HT-29 cells when stimulated with 1000 U/mL TGF-β for 24 h. The stimulation of HT-29 cells with IL1 α alone and IL1α- TGF-β combination has not revealed any effect on hCA9 expression in both levels of gene and protein in contrast to, 1000 U/mL IL1α-TNFα and especially TGFβ-TNFα have reducing effect on h CA9 expression level in HT-29 cells for time ranges of 24 h, 48 h, 72 h. In addition to this data, it was observed that HT-29 cells at the phase of G0G1 are arrested in cell cycle when stimulated with either of 1000 U/mL IL1α-TNFα and TGFβ-TNFα. Moreover, it was observed that h CA9 expression level in HT-29 cells decreases at the phases of synthesis (S) and G2M. Discussion: We concluded that combination of TNFα-TGFβ has created antagonistic effect on hCA9 expression in HT-29 colon cancer cell model. On the other hand, combination of TNFα-IL1α caused sinergistic effect on h CA9 expression level in this cell model. When these results are demonstrated decrease in the cytokine exposed hCA9 expression is a finding to develop a novel approach for anticancer therapy. Conclusion: Our finding related to the change in the expression of hCA9 following cytokine stimulate to colon cancer cell line gives an idea about the effect of cytokine stimulation on the expression of this gene which will be a hot spot research in colon carcinogenesis. Methods: HT-29 colon cells were chosen as a colorectal adenocarcinoma model. hCA9 gene expression in the level of mRNA was measured in cytokines stimulated HT-29 cells by Quantitative Real-time PCR. Meanwhile, hCAIX expression in the level of protein and cell cycle aassay were detected by flow cytometry.

scholarly journals In Vitro Evaluation of Sulforaphane and a Natural Analog as Potent Inducers of 5-Fluorouracil Anticancer Activity

Molecules ◽  
2018 ◽  
Vol 23 (11) ◽  
pp. 3040 ◽  
Author(s):  
Małgorzata Milczarek ◽  
Lidia Mielczarek ◽  
Katarzyna Lubelska ◽  
Aleksandra Dąbrowska ◽  
Zdzisław Chilmonczyk ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Anticancer Activity ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Natural Analog ◽  
Colon Cancer Cell Lines ◽  
The Impact

Isothiocyanates (R-NCS) are sulphur-containing phytochemicals. The main source are plants of the Brassicaceae family. The best known plant-derived isothiocyanate is sulforaphane that has exhibited anticancer activity in both in vivo and in vitro studies. Recent attempts to expand their use in cancer therapy involve combining them with standard chemotherapeutics in order to increase their therapeutic efficacy. The aim of this paper is to determine the impact of sulforaphane and its natural analog alyssin on the anticancer activity of the well-known anticancer drug 5-fluorouracil. The type of drug-drug interactions was determined in prostate and colon cancer cell lines. Confocal microscopy, western blot and flow cytometry methods were employed to determine the mechanism of cytotoxic and cytostatic action of the combinations. The study revealed that additive or synergistic interactions were observed between 5-fluorouracil and both isothiocyanates, which enhanced the anticancer activity of 5-fluorouracil, particularly in colon cancer cell lines. An increased cytostatic effect was observed in case of alyssin while for sulforaphane the synergistic interaction with 5-fluorouracil involved an intensification of apoptotic cell death.

Thymidylate synthase inhibition triggers apoptosis via caspases-8 and -9 in both wild-type and mutant p53 colon cancer cell lines

2003 ◽  
Vol 39 (9) ◽  
pp. 1310-1317 ◽  
Author(s):  
H.H.J Backus ◽  
D Wouters ◽  
C.G Ferreira ◽  
V.M.M van Houten ◽  
R.H Brakenhoff ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Thymidylate Synthase ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Mutant P53 ◽  
Wild Type ◽  
Colon Cancer Cell Lines

scholarly journals TRIM29 Reverses Oxaliplatin Resistance of P53 Mutant Colon Cancer Cell

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Guoqiong Lei ◽  
Sushun Liu ◽  
Xin Yang ◽  
Chao He
Keyword(s):  
Colon Cancer ◽  
Cancer Cell ◽  
Cell Model ◽  
P53 Protein ◽  
Underlying Mechanism ◽  
Resistant Cell ◽  
Colon Cancer Cell ◽  
Mutant P53 ◽  
Ht29 Cells ◽  
First Choice

Background. Oxaliplatin is the first-choice chemotherapy method for patients with advanced colon cancer. However, its resistance leads to treatment failure for many patients. In our experiments, we aim to elucidate the associations among TRIM29 protein, mutant P53, and the resistance of colon cancer cells to oxaliplatin. Methods. HCT116 and HT-29 cells were cultured and transfected with plasmids pIRES2-ZsGreen1-TRIM29-flag. Western blot and real-time qRT-PCR were utilized to examine the protein and mRNA expressions of TRIM29 and other related markers, respectively. MTT assay was utilized to determine the cell growth rate and generate the inhibition curve. Continuous culture in low-concentration oxaliplatin was conducted to construct oxaliplatin-resistant cell lines. The coimmunoprecipitation method and immunofluorescence detection were used to examine the interaction between TRIM29 and mutant P53 protein in HT29 cells. Results. We successfully transfected pIRES2-ZsGreen1-TRIM29-flag into HCT116 and HT29 cells, which were utilized in the whole experiments. TRIM29 significantly increased the sensitivity of P53 mutant colon cancer cell HT29 to oxaliplatin. The oxaliplatin-resistant model of P53 mutant colon cancer cell HT29 was successfully constructed. TRIM29 physically bound with mutant P53 and retained it in the cytoplasm from the nucleus, which inhibited its transcription function of downstream genes such as MDR1. In addition, TRIM29 successfully reversed the resistance of HT29-OX resistant cell model to oxaliplatin. Conclusion. In mutant P53 colon cancer cell HT29, TRIM29 greatly increased the sensitivity of HT29 to oxaliplatin and reverse oxaliplatin resistance. The underlying mechanism is TRIM29 may increase the sensitivity of HT29 to oxaliplatin by blocking the transcriptional function of mutant P53, which inhibits the transcription function of its downstream gene such as MDR1.

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