EFFECT OF VALPROIC ACID IN COMPARISON WITH VORINOSTAT ON CELL GROWTH INHIBITION AND APOPTOSIS INDUCTION IN THE HUMAN COLON CANCER SW48 CELLS IN VITRO

2018 ◽  
Vol 40 (2) ◽  
pp. 95-100 ◽  
Author(s):  
M Sanaei ◽  
F Kavoosi ◽  
O Mansoori
Keyword(s):  
Colon Cancer ◽  
Valproic Acid ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Histone Deacetylases ◽  
Regulation Of Gene Expression ◽  
Human Colon ◽  
Apoptosis Induction ◽  
Cell Growth Inhibition ◽  
Human Colon Cancer

Aim: Acetylation levels of histones are the result of the balance between histone acetyltransfrases and histone deacetylases activities, which plays an important role in chromatin remodeling and regulation of gene expression. Histone deacetylases inhibitors such as valproic acid, vorinostat have attracted interest because of their ability to induce differentiation and apoptosis of cancer cells. The current study was designed to assess the effect of valproic acid in comparison to and in combination with vorinostat on cell growth inhibition and apoptosis induction in the human colon cancer SW48 cells. Materials and Methods: The colon cancer SW48 cells were seeded and treated with various doses of valproic acid and vorinostat and MTT assay and flow cytometric assay were done to determine cell viability and cell apoptosis, respectively. Results: All concentrations of both agents reduced viability significantly in a dose- and time-dependent fashion (p < 0.004). Both compounds, either single or combined agents, induced apoptosis significantly, whereas the ratio of the apoptotic cells treated with combined agents was more significant than the single. Conclusion: Our findings suggest that vaproic acid and vorinostat can significantly inhibit cell growth and induce apoptosis in colon cancer SW48 cells.

Brosimone I, an isoprenoid-substituted flavonoid, induces cell cycle G1phase arrest and apoptosis through ROS-dependent endoplasmic reticulum stress in HCT116 human colon cancer cells

2019 ◽  
Vol 10 (5) ◽  
pp. 2729-2738 ◽  
Author(s):  
Yueliang Zhao ◽  
Yue Zhou ◽  
Mingfu Wang
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Endoplasmic Reticulum ◽  
Cell Growth ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Cell Growth Inhibition ◽  
Human Colon Cancer ◽  
Artocarpus Heterophyllus ◽  
Human Colon Cancer Cells

Brosimone I, an isoprenoid-substituted flavonoid fromArtocarpus heterophyllus, induces cell growth inhibition through the induction of ROS-mediated increased cytosolic Ca2+, ER stress, and the activation of the CaMKK-AMPK pathway.

scholarly journals Regulation of Butyrate-Induced Resistance through AMPK Signaling Pathway in Human Colon Cancer Cells

Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1604
Author(s):  
Hee Young Yoo ◽  
So Yeon Park ◽  
Sun-Young Chang ◽  
So Hee Kim
Keyword(s):  
Colon Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Histone Deacetylases ◽  
Chronic Exposure ◽  
Mammalian Target Of Rapamycin ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells

Butyrates inhibit cell growth in colon cancer cells by inhibiting histone deacetylases. However, chronic exposure to butyrates induces butyrate resistance in colon cancer cells. The mechanism underlying the acquisition of resistance is not yet fully understood. Here, butyrate-resistant (BR) colon cancer cells were developed in HCT116, HT29, and SW480 human colon cancer cells and were confirmed by the increase in the inhibitory concentrations of cell growth by 50% (IC50) compared to their respective parental (PT) cells. Chronic exposure to butyrate induced autophagy via higher expression of Beclin-1 and LC3B-II. The AMP-activated protein kinase (AMPK) was downregulated along with the activation of Akt and mammalian target of rapamycin (mTOR) and decrease in acetyl-CoA carboxylase (ACC) in BR colon cancer cells compared to those in their respective PT cells. Activation of AMPK by AICAR treatment in BR colon cancer cells suppressed cell proliferation by inhibiting Akt and mTOR and activating ACC. Taken together, chronic exposure to butyrate increased butyrate resistance in human colon cancer by inducing protective autophagy through the downregulation of AMPK/ACC and activation of Akt/mTOR signaling. Activation of AMPK restored sensitivity to butyrate by the inhibition of Akt/mTOR, suggesting that AMPK could be a therapeutic target for BR colon cancers.

scholarly journals Effect of 5-aza-2ˈ-deoxycytidine on p27Kip1, p21Cip1/Waf1/Sdi1, p57Kip2, and DNA methyltransferase 1 Genes Expression, Cell Growth Inhibition and Apoptosis Induction in Colon Cancer SW 480 and SW 948 Cell Lines

2020 ◽  
Vol 9 ◽  
pp. 1899
Author(s):  
Masumeh Sanaei ◽  
Fraidoon Kavoosi ◽  
Sedighe Nasiri
Keyword(s):  
Colon Cancer ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Cell Line ◽  
Cell Lines ◽  
Dna Methyltransferase ◽  
Dna Methyltransferase 1 ◽  
Apoptosis Induction ◽  
Cell Growth Inhibition ◽  
Genes Expression

Background: Dysregulation of the cell cycle has been reported in various cancers. Inactivation of the cyclin-dependent kinases inhibitors (CDKIs), CIP/KIP family, such as p21Cip1/Waf1/Sdi1, p27Kip1, and p57Kip2 genes because of hypermethylation has been shown in several cancers. Treatment with DNA demethylating agent 5-aza-2ˈ-deoxycytidine (5-Aza-CdR) has been indicated that affect genomic methylation and resulting in silenced genes reactivation in colon cancer. Previously, we evaluated the effect of 5-Aza-CdR on DNA methyltransferase 1 (DNMT1) gene expression in hepatocellular carcinoma (HCC) which encouraged us to design the current study. The present study aimed to evaluate the effect of 5-Aza-CdR on p21Cip1/Waf1/Sdi1, p27Kip1, p57Kip2, and DNAT1 genes expression, cell growth inhibition and apoptosis induction in colon cancer SW 480 and SW 948 cell lines. Materials and Methods: The effect of 5-aza-CdR on the SW 480 and SW 948 cells growth, apoptosis induction and genes expression were assessed by MTT assay, flow cytometry, and real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analysis respectively. Results: 5-aza-CdR inhibited cell growth as time- and dose-dependent manner significantly (P<0.001). The agent reactivated p15INK4, p16INK4, p18INK4, and p19INK4 genes expression and induced apoptosis at a concentration of 5 μM significantly. Besides, 5-aza-CdR had a more significant effect on the SW 480 cell line in comparison to SW 948 cell line. Conclusion: 5-Aza-CdR plays a key role in the up-regulation of p21Cip1/Waf1/Sdi1, p27Kip1, and p57Kip2 and down-regulation of DNMT1 genes resulting in cell growth inhibition and apoptosis induction. [GMJ.2020;9:e1899] DOI:10.31661/gmj.v9i0.1899

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.

Dimethyladamantylmaleimide-induced in vitro and in vivo growth inhibition of human colon cancer Colo205 cells

2002 ◽  
Vol 13 (5) ◽  
pp. 533-543 ◽  
Author(s):  
Jane-Jen Wang ◽  
Yaw-Terng Chern ◽  
Yuh-Fang Chang ◽  
Tsung-Yun Liu ◽  
Chin-Wen Chi
Keyword(s):  
Colon Cancer ◽  
Growth Inhibition ◽  
Human Colon ◽  
Human Colon Cancer ◽  
In Vivo Growth
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