2019
DOI: 10.1016/j.biopha.2019.109202
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An adenosine derivative (IFC-305) reduced the risk of radiation-induced intestinal toxicity in the treatment of colon cancer by suppressing the methylation of PPAR-r promoter

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Cited by 4 publications
(5 citation statements)
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“…5 -O-{[3-({4-[(3Aminopropyl)amino]butyl}amino)propyl]carbamoyl}-2 -deoxyadenosine is an adenosine derivative. Adenosine, an essential metabolite distributed in several mammalian tissues [57,58], acts as a ubiquitous endogenous cell signaling and modulator agent since it directly affects a variety of synaptic processes and signaling pathways, thus playing an important role in the regulation of several neurotransmitters in the central nervous system [59]. Moreover, adenosine produced in hypoxic, ischemic, or inflamed environments reduces tissue injury and promotes repair [60].…”
Section: Discussionmentioning
confidence: 99%
“…5 -O-{[3-({4-[(3Aminopropyl)amino]butyl}amino)propyl]carbamoyl}-2 -deoxyadenosine is an adenosine derivative. Adenosine, an essential metabolite distributed in several mammalian tissues [57,58], acts as a ubiquitous endogenous cell signaling and modulator agent since it directly affects a variety of synaptic processes and signaling pathways, thus playing an important role in the regulation of several neurotransmitters in the central nervous system [59]. Moreover, adenosine produced in hypoxic, ischemic, or inflamed environments reduces tissue injury and promotes repair [60].…”
Section: Discussionmentioning
confidence: 99%
“…It has been demonstrated that treatment with an adenosine aspartyl-derivative (IFC305) increases the MAT1A and decreases MAT2A levels, restoring transmethylation activities and facilitating chemoprotective effects against HCC [136]. These chemoprotective properties have been recently reported for colon cancer too [137]. Another purine whose abnormal levels contributes to tumor pathogenesis and progression is N6-Methyladenosine which is produced by the action of methyltransferases and removed by demethylases [138].…”
Section: Purines Signaling Hepatocarcinoma and Other Cancersmentioning
confidence: 99%
“…The treatment of colon cancer by suppressing the methylation of PPARγ promoter and enhancing PPARγ expression is also underway, because the hyper-methylation of promoter regions can induce PPARγ gene silence. Moreover, the risk of radiation-induced intestinal toxicity in methylated patients was also increased compared with un-methylated patients [81]. Furthermore, PPARβ is induced in intestinal stem cells and progenitor cells in high-fat diet-treated mice and enhances stemness and tumorigenicity of intestine [82].…”
Section: Ppars In Gastrointestinal Toxicitymentioning
confidence: 99%