Combined treatment with SAHA, bortezomib, and clarithromycin for concomitant targeting of aggresome formation and intracellular proteolytic pathways enhances ER stress-mediated cell death in breast cancer cells

Komatsu, Sumio; Moriya, Shota; Che, Xiaofang; Yokoyama, Tomohisa; Kohno, Norio; Miyazawa, Kenji

doi:10.1016/j.bbrc.2013.06.032

Cited by 39 publications

(38 citation statements)

References 26 publications

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“…Analogous results were obtained for MDA-MB-231 breast cancer cells with similar concentrations. 64 Nevertheless, the limited efficacy of combined treatment in urothelial carcinoma compared with other tumor types may be explained by tissue-dependent differences in proliferation rates and associated cellular stress caused by misfolded proteins. Our own observations and those published by Karkoulis et al 13 suggest that UPS stress might play a minor role in urothelial carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

Limited efficacy of specific HDAC6 inhibition in urothelial cancer cells

Rosik

Niegisch

Fischer

et al. 2014

Cancer Biology & Therapy

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Section: Discussionmentioning

confidence: 99%

Limited efficacy of specific HDAC6 inhibition in urothelial cancer cells

Rosik

Niegisch

Fischer

et al. 2014

Cancer Biology & Therapy

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“…This could suggest that resistant cells have a better capacity to respond to the drug also by increasing the protein-folding capacity in endoplasmic reticulum. In this regard, it has been recently shown that breast cancer cell cotreatments with SAHA and bortezomib, a proteasome inhibitor, enhance single treatment effects, inducing an endoplasmic reticulum stress-dependent cell death (28).…”

Section: Discussionmentioning

confidence: 99%

Redox-Mediated Suberoylanilide Hydroxamic Acid Sensitivity in Breast Cancer

Chiaradonna

Barozzi

Miccolo

et al. 2015

Antioxidants & Redox Signaling

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Aims: Vorinostat (suberoylanilide hydroxamic acid; SAHA) is a histone deacetylase inhibitor (HDACi) approved in the clinics for the treatment of T-cell lymphoma and with the potential to be effective also in breast cancer. We investigated the responsiveness to SAHA in human breast primary tumors and cancer cell lines. Results: We observed a differential response to drug treatment in both human breast primary tumors and cancer cell lines. Gene expression analysis of the breast cancer cell lines revealed that genes involved in cell adhesion and redox pathways, especially glutathione metabolism, were differentially expressed in the cell lines resistant to SAHA compared with the sensitive ones, indicating their possible association with drug resistance mechanisms. Notably, such an association was also observed in breast primary tumors. Indeed, addition of buthionine sulfoximine (BSO), a compound capable of depleting cellular glutathione, significantly enhanced the cytotoxicity of SAHA in both breast cancer cell lines and primary breast tumors. Innovation: We identify and validate transcriptional differences in genes involved in redox pathways, which include potential predictive markers of sensitivity to SAHA. Conclusion: In breast cancer, it could be relevant to evaluate the expression of antioxidant genes that may favor tumor resistance as a factor to consider for potential clinical application and treatment with epigenetic drugs (HDACis). Antioxid. Redox Signal. 23, 15-29.

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“…Inhibition of autophagy by 3-methyladenine, chloroquine or ATG5/Beclin1 silencing enhances cell death by NVP-BEZ235 combined with radiation. Clarithromycin, a macrolide antibiotic, has been reported to block autophagic flux [79,80]. In breast cancer cells clarithromycin enhances the cytotoxicity of the proteasome inhibitor bortezomib.…”

Section: Autophagy Induction Combined With Autophagy Inhibitionmentioning

confidence: 99%