Table 1.
Compound | Conc. | T286 dependent? a | Cell line | Proteasome inhibitor |
All-trans retinoic acid (RA) | 4–10 μM | Yes | BEAS-2B, NT2/D1 | Lactacystin, LLnLb |
Differentiation-inducing factor-1 and 3 (DIF-1 and DIF-3) | 30 μM | Yesc | SCC, HeLa | MG132 |
1-Methyl-4-phenylpyridinium ion (MPP+) | 300 nM | Yes | MG63 | MG132 |
hypothemycin | 0.5 μg/Ml | N.D. | NIH3T3-DT | Lactacystin |
O-methyl deoxybouvardin (RA-VII) | 100 nM | N.D. | DLD-1 | Lactacystin |
GL331 | 10 μM | N.D. | CL1-5 | N-CBZ-L-L-L-AL |
Resveratrol | 300 μM | N.D. | SW480 | LLnLb |
Diferuloylmethane (curcumin) | 25 μM | N.D. | LnCap, various breast cancer derived | Lactacystin |
Lovastatin | 10 μM | PC-3-M | LLnLb, d | |
Aspirin | 5 nmol/L | Yese | SW480, HT-29 | MG132 |
Cycloheximide | 50 μM | No | MCF-7 | MG132 |
15-deoxy-Δ12,14 prostaglandin J2 (PGJ2)f | 5–20 μM | N.D. | MCF-7 | MG132, PSII |
Ciglitazonef | 30–40 μM | N.D. | MCF-7 | MG132, PSII |
Troglitazonef | 40 μM | No | MCF-7 | MG132, lactacystin, epoxomicin |
Δ2-TGg | 5 μM | No | MCF-7 | MG132, lactacystin, epoxomicin |
Rapamycin | 100 nmol/L | Yes | MCF-7, MDA-MB-468 | LLnLb |
Trichostatin A (TSA)h | 1 μM | Yes/noi | MCF-7, MDA-MB-231, KNRK | MG132, ALLN, lactacystin, NLVSj |
Sodium chloride (NaCl), calcium chloride (CaCl2), magnesium chloride (MgCl2) | 50 mM | Yese | Granta 519 | LLnLb, lactacystin, MG132 |
a) T286 phosphorylation requirement, b) LLnL (ALLN, Calpain inhibitor 1, N-acetyl-leucyl-leucyl-norleucinal, MG101), c) Mirk/Dyrk 1b mediated T288 phosphorylation required, d) Lactacystin failed to abolish lovastatin induced cyclin D1 degradation, e) p38SAPK2 mediated T286 phosphorylation, f) PGJ2, ciglitazone and troglitazone are PPARγ agonists, g) Δ2-TG is structurally related to troglitazone but lacks PPARγ agonist activity, h) TSA is a prototype HDAC inhibitor, i) partial requirement for GSK3β in TSA induced cyclin D1 degradation, j) NLVS (NIP-leu3-vinyl sulphone)