2019
DOI: 10.1016/j.cbi.2019.04.004
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Inhibitors of aldehyde dehydrogenases of the 1A subfamily as putative anticancer agents: Kinetic characterization and effect on human cancer cells

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Cited by 20 publications
(28 citation statements)
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“…atRAL was freshly prepared on the day of an assay with concentration determined by absorption spectroscopy as previously described [54]. For determination of the effects of magnesium ions and His-tag on the activity of RALDHs/ALDH2, assays with 20 μl of 4.6 μM His-tagged or untagged enzyme in buffer E (final concentration: 460 nM), 20 μl of 1 mM NAD + (final concentration: 100 μM) and initiated by the addition of 20 μl of 120 μM atRAL substrate dissolved in ethanol (final concentration: 12 μM) were separately conducted in three HEPES-based buffers (total volume: 200 μl) with and without magnesium as follows: RB1 (20 mM HEPES pH 8.5, 150 mM KCl, 1 mM ethylenediaminetetraacetic acid (EDTA) and 20% 2-methyl-2,4-pentanediol (MPD) [20]), RB2 (50 mM HEPES pH 8.0, 50 mM KCl, 0.5 mM EDTA, 0.5 mM dithiothreitol (DTT) and 5% MPD) and RB3 (50 mM HEPES pH 8.0, 50 mM KCl, 0.5 mM EDTA, 0.5 mM DTT, 5% MPD and 30 mM MgCl 2 [55]). For determination of the effects of various spice and herb extracts on RALDHs/ALDH2, assays with 20 μl of 4.0 μM untagged enzyme in buffer E (final concentration: 400 nM), 20 μl of 1 mM NAD + (final concentration: 100 μM), 20 μl of extract (final concentration: 5% of reaction mixture) in ethanol 60% and initiated by the addition of 20 μl of 120 μM atRAL substrate dissolved in ethanol (final concentration: 12 μM) were conducted in RB1 for RALDH1/2 and ALDH2 or buffer RB3 for RALDH3 (total volume: 200 μl).…”
Section: Determination Of Enzyme Activity Of Raldhs/aldh2mentioning
confidence: 99%
“…atRAL was freshly prepared on the day of an assay with concentration determined by absorption spectroscopy as previously described [54]. For determination of the effects of magnesium ions and His-tag on the activity of RALDHs/ALDH2, assays with 20 μl of 4.6 μM His-tagged or untagged enzyme in buffer E (final concentration: 460 nM), 20 μl of 1 mM NAD + (final concentration: 100 μM) and initiated by the addition of 20 μl of 120 μM atRAL substrate dissolved in ethanol (final concentration: 12 μM) were separately conducted in three HEPES-based buffers (total volume: 200 μl) with and without magnesium as follows: RB1 (20 mM HEPES pH 8.5, 150 mM KCl, 1 mM ethylenediaminetetraacetic acid (EDTA) and 20% 2-methyl-2,4-pentanediol (MPD) [20]), RB2 (50 mM HEPES pH 8.0, 50 mM KCl, 0.5 mM EDTA, 0.5 mM dithiothreitol (DTT) and 5% MPD) and RB3 (50 mM HEPES pH 8.0, 50 mM KCl, 0.5 mM EDTA, 0.5 mM DTT, 5% MPD and 30 mM MgCl 2 [55]). For determination of the effects of various spice and herb extracts on RALDHs/ALDH2, assays with 20 μl of 4.0 μM untagged enzyme in buffer E (final concentration: 400 nM), 20 μl of 1 mM NAD + (final concentration: 100 μM), 20 μl of extract (final concentration: 5% of reaction mixture) in ethanol 60% and initiated by the addition of 20 μl of 120 μM atRAL substrate dissolved in ethanol (final concentration: 12 μM) were conducted in RB1 for RALDH1/2 and ALDH2 or buffer RB3 for RALDH3 (total volume: 200 μl).…”
Section: Determination Of Enzyme Activity Of Raldhs/aldh2mentioning
confidence: 99%
“…1) 18,19 . It has also been proposed that ALDH may directly metabolize chemotherapeutics, inactivating drugs such as cyclophosphamide, paclitaxel and doxorubicin before they can fulfill their intended purpose 20,21 . Due to these robust MDR mechanisms, ALDH expressing cell lines are resistant to several common chemotherapies, including etoposide, cisplatin, and fluorouracil 22 .…”
Section: Aldehyde Dehydrogenase As a Csc Markermentioning
confidence: 99%
“…Previous work showed that H2S may act a novel inhibitor of ALDH activity 20 . We expanded upon this finding and examined the effects of H2S on both ALDH activity and expression.…”
Section: H2s Inhibits Aldh Expression and Activitymentioning
confidence: 99%
“…Histological analysis of ALDH1 expression using lung tissue samples revealed a correlation between its expression and poor prognosis in patients with lung cancer [11][12][13]. Thus, inhibition of ALDH activity is expected to effectively eradicate the drug-tolerant CSC subpopulation during lung cancer treatment [14].…”
Section: Introductionmentioning
confidence: 99%