1993
DOI: 10.1097/00001813-199306000-00019
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Rhein inhibits glucose uptake in Ehrlich ascites tumor cells by alteration of membrane-associated functions

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Cited by 35 publications
(20 citation statements)
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“…This inhibition has been postulated to be an interaction of rhein with cell membranes that results in an alteration of membrane-associated functions. 58 Further study suggests that this anthraquinone induced enhancement in CD95 and its ligands, and subsequent apoptotic effect in HepG2 cells. 47 In addition, this anthraquinone induces apoptosis in HL-60 cells through the mitochondrial death pathway by causing the loss of mitochondrial membrane potential, cytochrome c release, and cleavage of Bid protein.…”
Section: Induction Of Apoptosismentioning
confidence: 90%
“…This inhibition has been postulated to be an interaction of rhein with cell membranes that results in an alteration of membrane-associated functions. 58 Further study suggests that this anthraquinone induced enhancement in CD95 and its ligands, and subsequent apoptotic effect in HepG2 cells. 47 In addition, this anthraquinone induces apoptosis in HL-60 cells through the mitochondrial death pathway by causing the loss of mitochondrial membrane potential, cytochrome c release, and cleavage of Bid protein.…”
Section: Induction Of Apoptosismentioning
confidence: 90%
“…Reports of the pharmacology of diacetyl rhein show that it can have a wide range of biological activity [12][13][14]. What is perhaps more significant is that using the protocol outlined in this paper, it is possible to determine the in vivo actions of various compounds on their ability to inhibit turnover.…”
Section: Inflamm Resmentioning
confidence: 96%
“…It has also been shown to influence cell growth and apoptosis in several human cancer cell lines such as cervical cancer Ca Ski (120), colon adenocarcinoma CaCo-2 (245), glioma U-373MG (74), hepatocellular carcinoma BEL-7402 (265), hepatoblastoma HepG2 (146), lung cancer A549 (108), promyelocytic leukemia HL-60 (181), and human tongue SSC-4 cancer cell lines (42,150). Moreover, rhein can inhibit the uptake and glycolysis of glucose and protein synthesis in cancer cells (29,30,73). Although it has been reported that increased expression of p53, p21, and CD96 may be responsible for the apoptosis of human hepatoblastoma HepG2 cell lines induced by rhein in a similar manner to AE (146), the molecular mechanisms by which rhein influences cell growth and apoptosis of cancer cells differ from AE.…”
Section: The Inhibitory Mechanisms Of Natural Compounds Against Npc Smentioning
confidence: 99%