title: Suberoylanilide hydroxamic acid induces apoptosis and sub-G1 arrest of 320 HSR colon cancer cells.
abstract: BACKGROUND
  Histone deacetylases and histone acetyl transferases covalently modify histone proteins, consequentially altering chromatin architecture and gene expression.
  
  
  METHODS
  The effects of suberoylanilide hydroxamic acid, a HDAC inhibitor, on 320 HSR colon cells were assessed in 320 HSR colon cancer cells.
  
  
  RESULTS
  Concentration and time-dependent inhibition of 320 HSR cell proliferation was observed. Treatment of 320 HSR cells with 5 μM SAHA for 72 h significantly inhibited their growth by 50% as compared to that of the control. Fluorescence-activated cell sorting analysis demonstrated significant inhibition of cell cycle progression (sub-G1 arrest) and induction of apoptosis upon various SAHA concentrations after 48 h. In addition, the anti-apoptosis proteins, survivin and Bcl-xL, were significantly inhibited by SAHA after 72 h of treatment. Immunocytochemistry analysis revealed that SAHA-resistant cells were positive for cyclin A (85%), ki-67 (100%), p53 (100%), survivin (100%), and p21 (90%) expression. Furthermore, a significant increase cyclin A-, Ki-67-, p53-, survivin-, and p21-positive cells were noted in SAHA-resistant tumor cells.
  
  
  CONCLUSIONS
  Our results demonstrated for the first time in 320 HSR colon adenocarcinoma cells that SAHA might be considered as an adjuvant therapy for colon adenocarcinoma.
authors.affiliation: Department of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taiwan, ROC.
authors.forename: Pei-Chang
authors.initials: PC
authors.lastname: Sun
authors.forename: Ching
authors.initials: C
authors.lastname: Tzao
authors.forename: Ban-Hen
authors.initials: BH
authors.lastname: Chen
authors.forename: Chen-Wei
authors.initials: CW
authors.lastname: Liu
authors.forename: Cheng-Ping
authors.initials: CP
authors.lastname: Yu
authors.forename: Jong-Shiaw
authors.initials: JS
authors.lastname: Jin
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D045744:Cell Line, Tumor / Q000187:drug effects / Q000502:physiology; D049109:Cell Proliferation / Q000187:drug effects; D002469:Cell Separation; D017024:Chemotherapy, Adjuvant; D005434:Flow Cytometry; D016193:G1 Phase / Q000187:drug effects*; D056572:Histone Deacetylase Inhibitors / Q000494:pharmacology*; D006801:Humans; D006877:Hydroxamic Acids / Q000494:pharmacology*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D000077337:Vorinostat
chemical_list: D000970:Antineoplastic Agents; D056572:Histone Deacetylase Inhibitors; D006877:Hydroxamic Acids; D042461:Vascular Endothelial Growth Factor A; D000077337:Vorinostat