apicidin and Prostatic-Neoplasms

apicidin has been researched along with Prostatic-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for apicidin and Prostatic-Neoplasms

Article	Year
Combination therapy induces unfolded protein response and cytoskeletal rearrangement leading to mitochondrial apoptosis in prostate cancer. Molecular oncology, 2016, Volume: 10, Issue:7 Development of therapeutic resistance is responsible for most prostate cancer (PCa) related mortality. Resistance has been attributed to an acquired or selected cancer stem cell phenotype. Here we report the histone deacetylase inhibitor apicidin (APC) or ER stressor thapsigargin (TG) potentiate paclitaxel (TXL)-induced apoptosis in PCa cells and limit accumulation of cancer stem cells. TXL-induced responses were modulated in the presence of TG with increased accumulation of cells at G1-phase, rearrangement of the cytoskeleton, and changes in cytokine release. Cytoskeletal rearrangement was associated with modulation of the cytoplasmic and mitochondrial unfolded protein response leading to mitochondrial dysfunction and release of proapoptotic proteins from mitochondria. TXL in combination with APC or TG enhanced caspase activation. Importantly, TXL in combination with TG induced caspase activation and apoptosis in X-ray resistant LNCaP cells. Increased release of transforming growth factor-beta (TGF-β) was observed while phosphorylated β-catenin level was suppressed with TXL combination treatments. This was accompanied by a decrease in the CD44(+)CD133(+) cancer stem cell-like population, suggesting treatment affects cancer stem cell properties. Taken together, combination treatment with TXL and either APC or TG induces efficient apoptosis in both proliferating and cancer stem cells, suggesting this therapeutic combination may overcome drug resistance and recurrence in PCa. Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; beta Catenin; Caspases; Cell Cycle Checkpoints; Cell Death; Cell Line, Tumor; Cytoskeleton; Enzyme Activation; G1 Phase; G2 Phase; HSP70 Heat-Shock Proteins; Humans; Interferon-gamma; Interleukin-8; Male; Matrix Metalloproteinases; Membrane Potential, Mitochondrial; Mitochondria; Neoplastic Stem Cells; Paclitaxel; Peptides, Cyclic; Phosphorylation; Prostatic Neoplasms; Reactive Oxygen Species; Thapsigargin; Transforming Growth Factor beta; Unfolded Protein Response; X-Rays	2016

Article

Year

Combination therapy induces unfolded protein response and cytoskeletal rearrangement leading to mitochondrial apoptosis in prostate cancer.

Molecular oncology, 2016, Volume: 10, Issue:7

Development of therapeutic resistance is responsible for most prostate cancer (PCa) related mortality. Resistance has been attributed to an acquired or selected cancer stem cell phenotype. Here we report the histone deacetylase inhibitor apicidin (APC) or ER stressor thapsigargin (TG) potentiate paclitaxel (TXL)-induced apoptosis in PCa cells and limit accumulation of cancer stem cells. TXL-induced responses were modulated in the presence of TG with increased accumulation of cells at G1-phase, rearrangement of the cytoskeleton, and changes in cytokine release. Cytoskeletal rearrangement was associated with modulation of the cytoplasmic and mitochondrial unfolded protein response leading to mitochondrial dysfunction and release of proapoptotic proteins from mitochondria. TXL in combination with APC or TG enhanced caspase activation. Importantly, TXL in combination with TG induced caspase activation and apoptosis in X-ray resistant LNCaP cells. Increased release of transforming growth factor-beta (TGF-β) was observed while phosphorylated β-catenin level was suppressed with TXL combination treatments. This was accompanied by a decrease in the CD44(+)CD133(+) cancer stem cell-like population, suggesting treatment affects cancer stem cell properties. Taken together, combination treatment with TXL and either APC or TG induces efficient apoptosis in both proliferating and cancer stem cells, suggesting this therapeutic combination may overcome drug resistance and recurrence in PCa.

Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; beta Catenin; Caspases; Cell Cycle Checkpoints; Cell Death; Cell Line, Tumor; Cytoskeleton; Enzyme Activation; G1 Phase; G2 Phase; HSP70 Heat-Shock Proteins; Humans; Interferon-gamma; Interleukin-8; Male; Matrix Metalloproteinases; Membrane Potential, Mitochondrial; Mitochondria; Neoplastic Stem Cells; Paclitaxel; Peptides, Cyclic; Phosphorylation; Prostatic Neoplasms; Reactive Oxygen Species; Thapsigargin; Transforming Growth Factor beta; Unfolded Protein Response; X-Rays

2016