MYC directs transcription of MCL1 and eIF4E genes to control sensitivity of gastric cancer cells toward HDAC inhibitors

MYC and EGR1 synergize to trigger tumor cell death by controlling NOXA and BIM transcription upon treatment with the proteasome inhibitor bortezomib

“…Viability of the cells was measured using MTT-assays (9). To determine Annexin V, cells were stained with propidium iodide (PI) and FITC-labeled anti-Annexin V using the Apoptosis Detection Kit I (BD Biosciences) and analyzed by FACS (23). Samples were analyzed using an FACScalibur flow cytometer (BD Biosciences) (23).…”

“…To determine Annexin V, cells were stained with propidium iodide (PI) and FITC-labeled anti-Annexin V using the Apoptosis Detection Kit I (BD Biosciences) and analyzed by FACS (23). Samples were analyzed using an FACScalibur flow cytometer (BD Biosciences) (23). A MoFlo (Beckman Coulter) cell sorter was used for sorting of red and/or green fluorescent cells.…”

“…A MoFlo (Beckman Coulter) cell sorter was used for sorting of red and/or green fluorescent cells. Caspase 3/7 activity was determined using Promega's Caspase-Glo 3/7 assay (23). …”

The Soy Isoflavone Equol May Increase Cancer Malignancy via Up-regulation of Eukaryotic Protein Synthesis Initiation Factor eIF4G

“…The c-Myc transcription factor is one of the most important somatically mutated oncogenes in human cancer and confers a selective advantage to cancer cells by promoting protein synthesis, proliferation, cell survival, differentiation, genetic instability, angiogenesis, hypoxia-mediated cancer progression, and metastasis (33,33,47,(62)(63)(64)(65)(66). Studies have shown that c-Myc up-regulates both eIF4E and eIF4G gene expression (58). Myc also has an IRES site and thus, in turn, is sensitive to elevated eIF4G and eIF4E levels (48).…”

Inhibition of histone deacetylase 4 increases cytotoxicity of docetaxel in gastric cancer cells

“…However, we tested the hypothesis that HDAC4 overexpression is essential for gastric tumor cell viability using the gastric cancer cell line SNU-16, which was specifically suited for this study because (i) the originating patient had limited prior therapy (no 5-fluorouracil/adriamycin/mitomycin-C treatment) [27], (ii) c-myc is amplified, which is a common event in gastric cancer (for review, see [28]) and which appears to repress the efficacy of the class I HDAC inhibitor vorinostat [29], and (iii) it has physiologic tumor levels of HDAC4 (Fig. 3A).…”