Histone deacetylase inhibitors induce apoptosis in both Type I and Type II endometrial cancer cells

Jiang, Shujuan; Dowdy, Sean C.; Meng, Xue; Wang, Zhaoyu; Jones, Monica B.; Podratz, Karl C.; Jiang, Shi Wen

doi:10.1016/j.ygyno.2007.01.012

Cited by 30 publications

(28 citation statements)

References 35 publications

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“…HDACIs induced mitochondrial membrane damage with concomitant cytochrome c release as well as apoptosis in a T-cell leukemia cell line and in various type I and type II endometrial cancers, including Ark2, Ishikawa, and AN3 cell lines. 65,66 As mentioned previously, HDACIs activate the mitochondrial apoptotic pathway by releasing cytochrome c from the mitochondrial intermembrane space and activating caspase-3. 67 Therefore, to further characterize the specific apoptotic pathways activated by TUB-A and PdNPs, we measured caspase-3 activity in cells that were subjected to single or combined drug treatment for 24 h, in the presence or absence of a caspase-3 inhibitor.…”

mentioning

confidence: 91%

Combination of palladium nanoparticles and tubastatin-A potentiates apoptosis in human breast cancer cells: a novel therapeutic approach for cancer

Yuan¹,

Peng²,

Gurunathan³

2017

IJN

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Background Breast cancer is the most common malignant disease that occurs in women. Histone deacetylase (HDAC) inhibition has recently emerged as an effective and attractive target for the treatment of cancer. The aim of this study was to investigate the efficacy of a combined treatment of tubastatin A (TUB-A) and palladium nanoparticles (PdNPs) against MDA-MB-231 human breast cancer cells using two different cytotoxic agents that work by two different mechanisms, thereby decreasing the probability of chemoresistance in cancer cells and increasing the efficacy of toxicity, to provide efficient therapy for advanced stage of cancer without any undesired side effects. Methods PdNPs were synthesized using a novel biomolecule called R-phycoerythrin and characterized using various analytical techniques. The combinatorial effect of TUB-A and PdNPs was assessed by various cellular and biochemical assays and also by gene expression analysis. Results The biologically synthesized PdNPs had an average size of 25 nm and were spherical in shape. Treatment of MDA-MB-231 human breast cancer cells with TUB-A or PdNPs showed a dose-dependent effect on cell viability. The combination of 4 μM TUB-A and 4 μM PdNPs had a significant inhibitory effect on cell viability compared with either TUB-A or PdNPs alone. The combinatorial treatment also had a more pronounced effect on the inhibition of HDAC activity and enhanced apoptosis by regulating various cellular and biochemical changes. Conclusion Our results suggest that there was a strong synergistic interaction between TUB-A and PdNPs in increasing apoptosis in human breast cancer cells. These data provide an important preclinical basis for future clinical trials on this drug combination. This combinatorial treatment increased therapeutic potentials, thereby demonstrating a relevant targeted therapy for breast cancer. Furthermore, we have provided the first evidence for the combinatorial effect and mechanism of toxicity of TUB-A and PdNPs in human breast cancer cells. The novelties of the study were identification of a combination therapy that consists of suitable therapeutic molecules that kill cancer cells and also exploration of two different possible mechanisms involved to reduce chemoresistance in cancer cells.

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mentioning

confidence: 91%

Combination of palladium nanoparticles and tubastatin-A potentiates apoptosis in human breast cancer cells: a novel therapeutic approach for cancer

Yuan¹,

Peng²,

Gurunathan³

2017

IJN

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“…There are two major types (I and II) of endometrial cancer with specific features and different changes in a genetic setting (21). HDAC inhibitors are an emerging class of targeted cancer therapeutics, and may have an important impact on the treatment of both types I and II endometrial carcinoma (22)(23)(24). Apicidin is a cyclic peptide group of HDAC inhibitors, and accounts for the in vitro high acetylation level of histones, which correlates with an increase in the transcription of various cancer-related genes (25).…”

Section: Discussionmentioning

confidence: 99%

Anti-tumor effect of apicidin on Ishikawa human endometrial cancer cells both in vitro and in vivo by blocking histone deacetylase 3 and 4

Kim

2009

Int J Oncol

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Abstract. Histone deacetylase (HDAC) inhibitors are a new class of anticancer agents that act by inhibiting cancer cell proliferation and inducing apoptosis both in vitro and in vivo. This study examined the anti-tumor effect of apicidin on human endometrial cancer Ishikawa cells in an animal model by inhibiting specific HDAC expression. Nude mice were injected subcutaneously (s.c.) with Ishikawa cells, and the levels of cell proliferation and apoptosis were measured in the tumor tissues after an apicidin treatment. The expression patterns of a specific HDAC class by apicidin were measured in Ishikawa endometrial cancer both in vitro and in vivo. The tumor volume and weight were measured after the apicidin treatment. Apicidin significantly increased the acetylated histone H3 levels in an Ishikawa cells in vitro culture but the levels of HDAC3 and HDAC4 expression were significantly decreased. Apicidin suppressed the tumor growth of transplanted Ishikawa cells, the expression of proliferative cell nuclear antigen (PCNA) and vascular endothelial growth factor (VEGF) in tumor xenograft model, respectively. The inhibitory effect of apicidin on tumor growth was mediated in part through the down-regulation of HDAC3 and HDAC4. We suggest that apicidin is an effective anti-tumor agent on human endometrial cancer cells, and acts by regulating cell proliferation and apoptosis through the down-regulation of HDAC3 and HDAC4.

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“…Docetaxel inhibits cell mitotic division and promotes apoptosis through stabilizing microtubule assembly. Our previous research shows that TSA and paclitaxel synergistically inhibits the proliferation of papillary serous endometrial cancer cells (Jiang et al, 2007). One of the key observations is that TSA combined with paclitaxel causes a marked increase of acetylated tubulin and microtubule stabilization.…”

Section: Introductionmentioning

confidence: 96%

“…One of the key observations is that TSA combined with paclitaxel causes a marked increase of acetylated tubulin and microtubule stabilization. The ability of TSA to potentiate the anticancer effects achieved by paclitaxel opens a new avenue to treat not only for women with endometrial cancer but also for patients with other malignancies with limited sensitivity to paclitaxel (Dowdy et al, 2006 ;Jiang et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Histone Deacetylase Inhibitor Trichostatin A Enhances Antitumor Effects of Docetaxel or Erlotinib in A549 Cell Line

Zhang

Jiang²,

Zhang³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Histone deacetylase inhibitors induce apoptosis in both Type I and Type II endometrial cancer cells

Cited by 30 publications

References 35 publications

Combination of palladium nanoparticles and tubastatin-A potentiates apoptosis in human breast cancer cells: a novel therapeutic approach for cancer

Combination of palladium nanoparticles and tubastatin-A potentiates apoptosis in human breast cancer cells: a novel therapeutic approach for cancer

Anti-tumor effect of apicidin on Ishikawa human endometrial cancer cells both in vitro and in vivo by blocking histone deacetylase 3 and 4

Histone Deacetylase Inhibitor Trichostatin A Enhances Antitumor Effects of Docetaxel or Erlotinib in A549 Cell Line

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