2005
DOI: 10.1016/j.bbalip.2005.01.008
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Increases in NMR-visible lipid and glycerophosphocholine during phenylbutyrate-induced apoptosis in human prostate cancer cells

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Cited by 84 publications
(103 citation statements)
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“…The rise in GPC is consistent with our previous findings in human colon cancer cells and has previously been observed with the histone deacetylase (HDAC) inhibitor and differentiating agent phenylbutyrate 50 as well as the early PI3K inhibitor LY294002. 51 Whether this effect is related to the molecular events triggered post-HSP90 inhibition or to reduced proliferation and/or the induction of differentiation observed in our melanoma cells post-exposure to HSP90 inhibitors remains to be established.…”
Section: ©2 0 1 1 L a N D E S B I O S C I E N C E D O N O T D I S Tsupporting
confidence: 80%
“…The rise in GPC is consistent with our previous findings in human colon cancer cells and has previously been observed with the histone deacetylase (HDAC) inhibitor and differentiating agent phenylbutyrate 50 as well as the early PI3K inhibitor LY294002. 51 Whether this effect is related to the molecular events triggered post-HSP90 inhibition or to reduced proliferation and/or the induction of differentiation observed in our melanoma cells post-exposure to HSP90 inhibitors remains to be established.…”
Section: ©2 0 1 1 L a N D E S B I O S C I E N C E D O N O T D I S Tsupporting
confidence: 80%
“…To check whether the resonances from this metabolite are indicative of a cell death process, cells were treated with phenylbutyrate (PB), a chemotherapeutic agent that has been shown to induce apoptosis in certain malignant cells. 26,27 The 1 H NMR spectrum after incubation with PB (10 mM) for 24 h showed also a profile for low cell density and viability and, additionally, a significant accumulation of mobile lipids ( Figure 4c). In agreement with our expectation, a high increased of the signals assigned to acetyl-CoA was also observed (peaks at 2.24 and 0.67 ppm).…”
Section: Resultsmentioning
confidence: 99%
“…In the case of phenylbutyrate, the rise in GPC levels was associated with mobile lipid accumulation and postulated to occur as a result of PLA2 activation (Milkevitch et al, 2005). The indomethacin-induced increase in cellular GPC was also attributed to enhanced membrane turnover through phospholipses (Glunde et al, 2006).…”
Section: Choline Phospholipid Metabolismmentioning
confidence: 91%