Induction of Apoptosis by the Medium-Chain Length Fatty Acid Lauric Acid in Colon Cancer Cells due to Induction of Oxidative Stress

Chemotherapy ◽  
2013 ◽  
Vol 59 (3) ◽  
pp. 214-224 ◽  
Author(s):  
J.K. Fauser ◽  
G.M. Matthews ◽  
A.G. Cummins ◽  
G.S. Howarth
Keyword(s):  
Oxidative Stress ◽  
Colon Cancer ◽  
Fatty Acid ◽  
Cancer Cells ◽  
Chain Length ◽  
Lauric Acid ◽  
Colon Cancer Cells ◽  
Medium Chain ◽  
Medium Chain Length ◽  
Induction Of Apoptosis

scholarly journals Remodeling of energy metabolism by a ketone body and medium-chain fatty acid suppressed the proliferation of CT26 mouse colon cancer cells

2017 ◽  
Vol 14 (1) ◽  
pp. 673-680 ◽  
Author(s):  
Yui Kadochi ◽  
Shiori Mori ◽  
Rina Fujiwara-Tani ◽  
Yi Luo ◽  
Yukiko Nishiguchi ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Fatty Acid ◽  
Energy Metabolism ◽  
Cancer Cells ◽  
Ketone Body ◽  
Chain Fatty Acid ◽  
Medium Chain Fatty Acid ◽  
Colon Cancer Cells ◽  
Medium Chain ◽  
Mouse Colon

scholarly journals Pro-Apoptotic Activity of Artichoke Leaf Extracts in Human HT-29 and RKO Colon Cancer Cells

2021 ◽  
Vol 18 (8) ◽  
pp. 4166
Author(s):  
Milena Villarini ◽  
Mattia Acito ◽  
Raffaella di Vito ◽  
Samuele Vannini ◽  
Luca Dominici ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Chlorogenic Acid ◽  
Cancer Cells ◽  
Herbaceous Plant ◽  
Colon Cancer Cells ◽  
Leaf Extracts ◽  
Caffeoylquinic Acids ◽  
Induction Of Apoptosis ◽  
Ht 29

(1) Background: Cynara cardunculus L. subsp. scolymus (L.) Hegi, popularly known as artichoke, is an herbaceous plant belonging to the Asteraceae family. Artichoke leaf extracts (ALEs) have been widely used in traditional medicine because of their hepatoprotective, cholagogic, hypoglycaemic, hypolipemic and antibacterial properties. ALEs are also recognized for their antioxidative and anti-inflammatory activities. In this study, we evaluated the cytotoxic, genotoxic, and apoptotic activities, as well as effect on cell growth of ALEs on human colon cancer HT-29 and RKO cells. HT-29 and RKO cells exhibit a different p53 status: RKO cells express the wild-type protein, whereas HT-29 cells express a p53-R273H contact mutant. (2) Methods: Four different ALEs were obtained by sequential extraction of dried artichoke leaves; ALEs were characterized for their content in chlorogenic acid, cynaropicrin, and caffeoylquinic acids. HT-29 and RKO cells were used for in vitro testing (i.e., cytotoxicity and genotoxicity assessment, cell cycle analysis, apoptosis induction). (3) Results: Two out of the four tested ALEs showed marked effects on cell vitality toward HT-29 and RKO tumour cells. The effect was accompanied by a genotoxic activity exerted at a non-cytotoxic concentrations, by a significant perturbation of cell cycle (i.e., with increase of cells in the sub-G1 phase), and by the induction of apoptosis. (4) Conclusions: ALEs rich in cynaropicrin, caffeoylquinic acids, and chlorogenic acid showed to be capable of affecting HT-29 and RKO colon cancer cells by inducing favourable biological effects: cell cycle perturbation, activation of mitochondrial dependent pathway of apoptosis, and the induction of genotoxic effects probably mediated by the induction of apoptosis. Taken together, these results weigh in favour of a potential cancer chemotherapeutic activity of ALEs.

scholarly journals Effects of propionate and carnitine on the hepatic oxidation of short- and medium-chain-length fatty acids

1988 ◽  
Vol 250 (3) ◽  
pp. 819-825 ◽  
Author(s):  
E P Brass ◽  
R A Beyerinck
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Organic Acid ◽  
Chain Length ◽  
Ketone Body ◽  
Acetyl Coa ◽  
Body Formation ◽  
Medium Chain ◽  
Medium Chain Length ◽  
Hepatic Oxidation

Accumulation of propionate, or its metabolic product propionyl-CoA, can disrupt normal cellular metabolism. The present study examined the effects of propionate, or propionyl-CoA generated during the oxidation of odd-chain-length fatty acids, on hepatic oxidation of short- and medium-chain-length fatty acids. In isolated hepatocytes, ketone-body formation from odd-chain-length fatty acids was slow as compared with even-chain-length fatty acid substrates, and increased as the carbon chain length was increased from five to seven to nine. In contrast, rates of ketogenesis from butyrate, hexonoate and octanoate were all approximately equal. Propionate (10 mM) inhibited ketogenesis from butyrate, hexanoate and octanoate by 81%, 53% and 18% respectively. Addition of carnitine had no effect on ketogenesis from the even-chain-length fatty acids, but increased the rate of ketone-body formation from pentanoate (by 53%), heptanoate (by 28%) and from butyrate or hexanoate in the presence of propionate. The inhibitory effect of propionate could not be explained by shunting acetyl-CoA into the tricarboxylic acid cycle, as CO2 formation from butyrate was also decreased by propionate. Examination of the hepatocyte CoA pool during oxidation of butyrate demonstrated that addition of propionate decreased acetyl-CoA and CoA as propionyl-CoA accumulated. Addition of carnitine decreased propionyl-CoA by 50% (associated with production of propionylcarnitine) and increased acetyl-CoA and CoA. Similar changes in the CoA pool were seen during the oxidation of pentanoate. These results demonstrate that accumulation of propionyl-CoA results in inhibition of short-chain fatty acid oxidation. Carnitine can partially reverse this inhibition. Changes in the hepatocyte CoA pool are consistent with carnitine acting by generating propionylcarnitine, thereby decreasing propionyl-CoA and increasing availability of free CoA. The data provide further evidence of the potential cellular toxicity from organic acid accretion, and supports the concept that carnitine's interaction with the cellular CoA pool can have a beneficial effect on cellular metabolism and function under conditions of unusual organic acid accumulation.

scholarly journals Identification and Characterization of a New Enoyl Coenzyme A Hydratase Involved in Biosynthesis of Medium-Chain-Length Polyhydroxyalkanoates in Recombinant Escherichia coli

2003 ◽  
Vol 185 (18) ◽  
pp. 5391-5397 ◽  
Author(s):  
Si Jae Park ◽  
Sang Yup Lee
Keyword(s):  
Escherichia Coli ◽  
Fatty Acid ◽  
Chain Length ◽  
Biosynthetic Pathway ◽  
Pha Synthase ◽  
Enzymatic Analysis ◽  
E Coli ◽  
Medium Chain ◽  
Medium Chain Length ◽  
Enoyl Coa Hydratase

ABSTRACT The biosynthetic pathway of medium-chain-length (MCL) polyhydroxyalkanoates (PHAs) from fatty acids has been established in fadB mutant Escherichia coli strain by expressing the MCL-PHA synthase gene. However, the enzymes that are responsible for the generation of (R)-3-hydroxyacyl coenzyme A (R3HA-CoAs), the substrates for PHA synthase, have not been thoroughly elucidated. Escherichia coli MaoC, which is homologous to Pseudomonas aeruginosa (R)-specific enoyl-CoA hydratase (PhaJ1), was identified and found to be important for PHA biosynthesis in a fadB mutant E. coli strain. When the MCL-PHA synthase gene was introduced, the fadB maoC double-mutant E. coli WB108, which is a derivative of E. coli W3110, accumulated 43% less amount of MCL-PHA from fatty acid compared with the fadB mutant E. coli WB101. The PHA biosynthetic capacity could be restored by plasmid-based expression of the maoCEc gene in E. coli WB108. Also, E. coli W3110 possessing fully functional β-oxidation pathway could produce MCL-PHA from fatty acid by the coexpression of the maoCEc gene and the MCL-PHA synthase gene. For the enzymatic analysis, MaoC fused with His6-Tag at its C-terminal was expressed in E. coli and purified. Enzymatic analysis of tagged MaoC showed that MaoC has enoyl-CoA hydratase activity toward crotonyl-CoA. These results suggest that MaoC is a new enoyl-CoA hydratase involved in supplying (R)-3-hydroxyacyl-CoA from the β-oxidation pathway to PHA biosynthetic pathway in the fadB mutant E. coli strain.

scholarly journals PKCζ Phosphorylates SIRT6 to Mediate Fatty Acid β-Oxidation in Colon Cancer Cells

Neoplasia ◽  
2019 ◽  
Vol 21 (1) ◽  
pp. 61-73 ◽  
Author(s):  
Tian Gao ◽  
Meiting Li ◽  
Guanqun Mu ◽  
Tianyun Hou ◽  
Wei-Guo Zhu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Fatty Acid ◽  
Cancer Cells ◽  
Colon Cancer Cells

scholarly journals [Corrigendum] A combination of inhibitors of glycolysis, glutaminolysis and de�novo fatty acid synthesis decrease the expression of chemokines in human colon cancer cells

2020 ◽  
Author(s):  
Alejandro Schcolnik‑Cabrera ◽  
Guadalupe Dominguez‑G�mez ◽  
Alma Ch�vez‑Blanco ◽  
Marisol Ram�rez‑Yautentzi ◽  
Roc�o Morales‑B�rcenas ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Fatty Acid ◽  
Cancer Cells ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Human Colon ◽  
Acid Synthesis ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells
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