scholarly journals Induction of a less aggressive phenotype in human colon carcinoma HCT116 cells by chronic exposure to HDAC inhibitor SAHA

2010 ◽  
Vol 24 (5) ◽  
Author(s):  
Binaschi
Keyword(s):  
Colon Carcinoma ◽  
Hdac Inhibitor ◽  
Chronic Exposure ◽  
Human Colon ◽  
Aggressive Phenotype ◽  
Human Colon Carcinoma ◽  
Hct116 Cells

scholarly journals Curcumin Downregulates Human GM3 Synthase (hST3Gal V) Gene Expression with Autophagy Induction in Human Colon Carcinoma HCT116 Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Miri Lee ◽  
Hyunju Choi ◽  
Kyoung-Sook Kim ◽  
Dong-Hyun Kim ◽  
Cheorl-Ho Kim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colon Carcinoma ◽  
Human Colon ◽  
Luciferase Reporter ◽  
Gm3 Synthase ◽  
Human Colon Carcinoma ◽  
Autophagy Induction ◽  
Promoter Deletion Analysis ◽  
V Gene ◽  
Hct116 Cells

Our recent report showed that curcumin, polyphenolic compound isolated from the herb Curcuma longa, upregulated the gene expression of human GD3 synthase (hST8Sia I) responsible for ganglioside GD3 synthesis with autophagy induction in human lung adenocarcinoma A549 cells. In this study, on the contrary to this finding, we demonstrated that curcumin downregulated the gene expression of human GM3 synthase (hST3Gal V) catalyzing ganglioside GM3 synthesis with autophagy induction in human colon carcinoma HCT116 cells. To clarify the mechanism leading to the downregulation of hST3Gal V gene expression in curcumin-treated HCT116 cells, we analyzed the curcumin-inducible promoter of the hST3Gal V gene by luciferase reporter assays. Promoter deletion analysis demonstrated that the -177 to -83 region, which includes putative binding sites for transcription factors NFY, CREB/ATF, SP1, EGR3, and MZF1, acts as the curcumin-responsive promoter of the hST3Gal V gene. Site-directed mutagenesis and chromatin immunoprecipitation analysis demonstrated that the CREB/ATF binding site at -143 is pivotal for curcumin-induced downregulation of hST3Gal V gene in HCT116 cells. The transcriptional activation of hST3Gal V in HCT116 cells was significantly repressed by an inhibitor of AMP-activated protein kinase (AMPK). These results suggest that AMPK signal pathway mediates hST3Gal V gene expression in HCT116 cells.

Cytotoxicity of New Ferulic-Acid Derivatives on Human Colon Carcinoma (HCT116) Cells

2019 ◽  
Vol 53 (6) ◽  
pp. 516-520
Author(s):  
L. A. Bakholdina ◽  
A. A. Markova ◽  
A. I. Khlebnikov ◽  
V. P. Sevodin
Keyword(s):  
Ferulic Acid ◽  
Colon Carcinoma ◽  
Human Colon ◽  
Human Colon Carcinoma ◽  
Hct116 Cells

Hypoxia and antioxidant signaling in human colon carcinoma HCT116 cells exposed in vitro to 64-Cu

2021 ◽  
Author(s):  
Gina Manda ◽  
Dana Niculae ◽  
Ionela-Victoria Neagoe ◽  
Radu Serban ◽  
Dragos-Andrei Niculae ◽  
...  
Keyword(s):  
Colon Carcinoma ◽  
Human Colon ◽  
Human Colon Carcinoma ◽  
Hct116 Cells

scholarly journals Nocodazole-induced p53-dependent c-Jun N-terminal Kinase Activation Reduces Apoptosis in Human Colon Carcinoma HCT116 Cells

2002 ◽  
Vol 277 (46) ◽  
pp. 43648-43658 ◽  
Author(s):  
Hong Zhang ◽  
Xiaoqing Shi ◽  
Qian-Jin Zhang ◽  
Maggie Hampong ◽  
Harry Paddon ◽  
...  
Keyword(s):  
Colon Carcinoma ◽  
Human Colon ◽  
Kinase Activation ◽  
Human Colon Carcinoma ◽  
Hct116 Cells

scholarly journals Inhibitor of protein kinases 1-(4-chlorobenzyl)-3-chloro-4-(3-trifluoromethylphenylamino)-1Н-pyrrole-2,5-dione induces DNA damage and apoptosis in human colon carcinoma cells

2020 ◽  
Vol 14 (4) ◽  
pp. 3-14
Author(s):  
N. S. Finiuk ◽  
◽  
O. Yu. Klyuchivska ◽  
H. M. Kuznietsova ◽  
S. P. Vashchuk ◽  
...  
Keyword(s):  
Western Blot ◽  
Dna Fragmentation ◽  
Colon Carcinoma ◽  
Human Colon ◽  
Carcinoma Cells ◽  
Strand Breaks ◽  
Colon Carcinoma Cells ◽  
Human Colon Carcinoma ◽  
Single Strand Breaks ◽  
Hct116 Cells

Background. The heterocyclic scaffolds are in the list of key structural blocks used at synthesis of novel biologically active compounds. Materials and Methods. The present study addressed the evaluation of the mecha­nisms of the DNA damaging and pro-apoptotic actions in vitro of the maleimide derivative 1-(4-chlorobenzyl)-3-chloro-4-(3-trifluoromethylphenylamino)-1Н-pyrrole-2,5-dione (MI-1) targeting human colon carcinoma cells of HCT116 line. The Western-blot analysis was used to study changes in apoptosis-associated proteins, DNA comet assay under alkaline conditions was applied for evaluation of the DNA-damaging events, and Barton’s assay with diphenylamine was applied for measuring the level of DNA fragmentation in human colon carcinoma cells treated with MI-1 compound. Results. The results of the Western-blot analysis demonstrated that MI-1 induced the apoptosis in HCT116 cells via mitochondria-dependent pathway. It activated caspase 3 via its cleavage in the treated human colon carcinoma cells. Besides, MI-1 increased the content of mitochondria-specific proteins: endonuclease G (EndoG) and the pro-apoptotic cytosolic protein protease-activating factor 1 (Apaf1). At the same time, MI-1 reduced the level of the anti-apoptotic Bcl-2 protein in HCT116 cells. The DNA comet analysis under alkaline conditions of the targeted human colon carcinoma cells of HCT116 line demonstrated that MI-1 induced DNA single-strand breaks in line with the olive tail moment of 13.2. The results of the colorimetric diphenylamine assay in HCT116 cells have shown that cell treatment with MI-1 increased the content of fragmented DNA to 14.2 %. Conclusions. The anti-proliferative action of MI-1 in human colon carcinoma cells of HCT116 line is associated with apoptosis induction via mitochondria-dependent pathway, as well as the DNA damage through single-strand breaks and DNA fragmentation. These data suggest that the 1-(4-chlorobenzyl)-3-chloro-4-(3-trifluoromethylpheny­l­amino)-1Н-pyrrole-2,5-dione (MI-1) might be a promising agent for suppression of growth of colon tumor cells. Keywords: 1Н-pyrrole-2,5-diones, apoptosis, Western-blot assay, comet assay, single-strand breaks, Barton’s assay, DNA fragmentation

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