In human CEM leukemia cells, etoposide reduced CCK-8 viability after 8 h, with a reported cellular IC50 of ∼10 μM. This value is specific to the cell model, assay and exposure period. [1]
Etoposide (500 μM, 8 h) was used to induce apoptosis in Caco-2 monolayers. Extrusion of cleaved-caspase-3-positive cells was less efficient in MRLC-DD-expressing monolayers than in controls. The authors explicitly report using Adooq A10373 for this application. [2]
Persistence of etoposide-stabilized human topoisomerase II cleavage complexes
Biochemical assay · Purified human topoisomerase IIα or IIβ with negatively supercoiled pBR322 DNA [1]
After equilibration with etoposide and tenfold dilution, enzyme-associated DNA breaks persisted longer than with genistein. The reported decay half-lives differed by isoform; these are cleavage-complex persistence endpoints, not IC50 values.
Literature-Reported Treatment Conditions
- Treatment concentration
- 50 μM before tenfold dilution
- Exposure duration
- 6 min to establish cleavage equilibrium; post-dilution time course up to 30 min
- Method
- Cell-free DNA cleavage/dilution assay
- Vehicle
- Stock in 100% DMSO (20 mM); final assay DMSO fraction not specified.
- Co-treatment
- None in adopted etoposide treatment; comparator groups are separate treatments.
- Reported limits
- Exact drug dissociation rates were not measured. Do not interpret decay half-lives as binding constants.
Methods and source locations
Compound reported in the paper: Etoposide (VP-16); Compound label in the paper: etoposide
Reported etoposide experiment only; no salt conversion or batch equivalence inferred.
Materials and Methods: Persistence of Topoisomerase II-DNA Cleavage Complexes in Vitro; Results and Figure 7
Persistence of topoisomerase II-associated double-stranded DNA breaks after dilution: Agarose-gel quantification of linear DNA after tenfold dilution; pre-dilution cleavage set to 100%; error bars SD, three independent experiments. — Results paragraph immediately before Figure 7; Figure 7 and caption
Etoposide reduces CEM cell viability after an 8-hour exposure
Cell-based study · Human CEM leukemia cells [1]
Etoposide reduced CCK-8 viability with a reported IC50 of ∼10 μM, compared with ∼180 μM for genistein in this assay. The number describes this cellular endpoint and exposure time, not biochemical enzyme potency.
Literature-Reported Treatment Conditions
- Treatment concentration
- 0–200 μM
- Exposure duration
- 8 h
- Method
- CCK-8 cell viability assay
- Vehicle
- 20 mM DMSO stock; final vehicle fraction not specified.
- Co-treatment
- None in adopted etoposide treatment; comparator groups are separate treatments.
- Reported limits
- Viability assay is a metabolic readout, not a direct count of apoptotic cells. No exact IC50 confidence interval reported in the read Results.
Methods and source locations
Compound reported in the paper: Etoposide (VP-16); Compound label in the paper: etoposide
Reported etoposide experiment only; no salt conversion or batch equivalence inferred.
Cell Viability Assay; Results: Figure 2 left panel and associated IC50 paragraph
CCK-8 cell viability relative to no-drug control: CCK-8, 450 nm; no-drug cultures set to 100%; error bars SD for three independent experiments. Genistein comparator IC50 ∼180 μM reported in Results. — Results paragraph referring to Figure 2 left panel; Figure 2 caption
Etoposide-induced apoptotic extrusion in Caco-2 monolayers
Cell-based study · Control and phosphomimetic MRLC-DD-expressing Caco-2 epithelial monolayers [2]
Etoposide was used to induce sporadic apoptosis. Among cleaved-caspase-3-positive cells, extrusion efficiency was lower in MRLC-DD monolayers than in control monolayers under the same etoposide exposure. This is a comparison of extrusion among apoptotic cells, not a drug cytotoxicity IC50 or proof of unchanged apoptosis rates.
Literature-Reported Treatment Conditions
- Treatment concentration
- 500 μM
- Exposure duration
- 8 h
- Method
- Etoposide treatment at 37°C followed by fixation and immunostaining; compare etoposide-exposed control and MRLC-DD monolayers
- Co-treatment
- None in adopted etoposide treatment; comparator groups are separate treatments.
- Reported limits
- Vehicle not identified in selected methods. S2 apoptosis-rate control referenced in Results but supplement not retrieved; no claim of equivalent apoptosis rates adopted.
Methods and source locations
Compound reported in the paper: Etoposide (VP-16); Compound label in the paper: etoposide
Reported etoposide experiment only; no salt conversion or batch equivalence inferred.
Figure 2A–B and caption; Results: global increase in baseline junctional tension; Methods: Induction of apoptosis and Extrusion analysis
Percentage of cleaved-caspase-3-positive cells successfully extruded above the apical monolayer plane: ZO-1/cleaved-caspase-3/DAPI confocal scoring; Figure 2B mean ± SEM; n ≥ 3 independent experiments; unpaired Student’s t test. No exact bar percentages extracted. — Figure 2A–B and caption; Methods: Extrusion analysis
