Continuous intracranial administration of suberoylanilide hydroxamic acid (SAHA) inhibits tumor growth in an orthotopic glioma model

2007 ◽  
Vol 83 (3) ◽  
pp. 267-275 ◽  
Author(s):  
Hasan C. Ugur ◽  
Naren Ramakrishna ◽  
Lorenzo Bello ◽  
Lata G. Menon ◽  
Seung-Ki Kim ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Hydroxamic Acid ◽  
Suberoylanilide Hydroxamic Acid ◽  
Glioma Model ◽  
Orthotopic Glioma

Temozolomide/PLGA microparticles plus vatalanib inhibits tumor growth and angiogenesis in an orthotopic glioma model

2010 ◽  
Vol 76 (3) ◽  
pp. 371-375 ◽  
Author(s):  
Yu-Hui Zhang ◽  
Zhi-Jian Yue ◽  
He Zhang ◽  
Gu-Sheng Tang ◽  
Yang Wang ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Plga Microparticles ◽  
Glioma Model ◽  
Orthotopic Glioma

scholarly journals Suberoylanilide hydroxamic acid (SAHA) causes tumor growth slowdown and triggers autophagy in glioblastoma stem cells

Autophagy ◽  
2013 ◽  
Vol 9 (10) ◽  
pp. 1509-1526 ◽  
Author(s):  
Ming-Tsang Chiao ◽  
Wen-Yu Cheng ◽  
Yi-Chin Yang ◽  
Chiung-Chyi Shen ◽  
Jiunn-Liang Ko
Keyword(s):  
Stem Cells ◽  
Tumor Growth ◽  
Hydroxamic Acid ◽  
Suberoylanilide Hydroxamic Acid ◽  
Glioblastoma Stem Cells

scholarly journals Suberoylanilide hydroxamic acid enhances the radiosensitivity of lung cancer cells through acetylated wild-type and mutant p53-dependent modulation of mitochondrial apoptosis

2021 ◽  
Vol 49 (2) ◽  
pp. 030006052098154
Author(s):  
Kan Wu ◽  
Xueqin Chen ◽  
Xufeng Chen ◽  
Shirong Zhang ◽  
Yasi Xu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Hydroxamic Acid ◽  
Site Directed Mutagenesis ◽  
Lung Cancer Cells ◽  
Mutant P53 ◽  
Suberoylanilide Hydroxamic Acid ◽  
Mitochondrial Apoptosis ◽  
Wild Type ◽  
Clonogenic Cell

Objective Suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor, has shown potential as a candidate radiosensitizer for many types of cancers. This study aimed to explore the radiosensitization mechanism of SAHA in lung cancer cells. Methods Mutations in p53 were generated by site-directed mutagenesis using polymerase chain reaction. Transfection was performed to generate H1299 cells carrying wild-type or mutant p53. The radiosensitizing enhancement ratio was determined by clonogenic assays. Mitochondrial apoptosis was detected using JC-1 staining and flow cytometry analysis. Results Our results showed that SAHA induced radiosensitization in H1299 cells expressing wild-type p53, p53R175H or p53P223L, but this enhanced clonogenic cell death was not observed in parental H1299 (p53-null) cells or H1299 cells expressing p53 with K120R, A161T and V274R mutations. In SAHA-sensitized cells, mitochondrial apoptosis was induced following exposure to irradiation. Additionally, we observed that a secondary mutation at K120 (K120R) could eliminate p53-mediated radiosensitization and mitochondrial apoptosis. Conclusions The results of this study suggest that wild-type and specific mutant forms of p53 mediate SAHA-induced radiosensitization by regulating mitochondrial apoptosis, and the stabilization of K120 acetylation by SAHA is the molecular basis contributing to radiosensitization in lung cancer cells.

Prenatal exposure to suberoylanilide hydroxamic acid perturbs corticogenesis

2013 ◽  
Vol 77 (1-2) ◽  
pp. 42-49 ◽  
Author(s):  
Nunung Yuniarti ◽  
Berry Juliandi ◽  
Chai MuhChyi ◽  
Hirofumi Noguchi ◽  
Tsukasa Sanosaka ◽  
...  
Keyword(s):  
Prenatal Exposure ◽  
Hydroxamic Acid ◽  
Suberoylanilide Hydroxamic Acid
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