PMID- 16360016
OWN - NLM
STAT- MEDLINE
DCOM- 20060321
LR  - 20111117
IS  - 0161-5890 (Print)
IS  - 0161-5890 (Linking)
VI  - 43
IP  - 6
DP  - 2006 Feb
TI  - Oct-1 DNA binding activity unresponsive to retinoblastoma protein expression 
      prevents MHC class II induction in a non-small cell lung carcinoma cell line.
PG  - 710-6
AB  - Numerous human tumor lines fail to induce major histocompatibility (MHC) class II 
      expression following interferon-gamma (IFN-gamma) treatment, a response that is 
      considered to be a normal function for almost all human parenchymal and 
      connective tissue cell-types. The effect of MHC class II non-inducibility on 
      solid tumor growth is controversial, but an extensive body of literature 
      indicates that tumor cell MHC class II expression can lead to an antitumor 
      response or tumor tolerance, depending on a number of variables. Thus, 
      understanding the molecular basis for MHC class II induction failures in solid 
      tumor cells will likely lead to ideas for manipulating the antitumor immune 
      response. To date, a handful of tumor associated molecular anomalies have 
      accounted for all the known failures of MHC class II inducibility. In particular, 
      lack of the retinoblastoma tumor suppressor protein (Rb) has been shown in both 
      human and mouse cells to be strongly associated with failure to induce MHC class 
      II. The basis for this relationship is traceable to, among other things, high 
      level Oct-1 DNA binding activity in Rb-defective cells, which represses the 
      prototypical human MHC class II gene, HLA-DRA. Ordinarily, re-establishment of Rb 
      expression leads to elimination of, or substantially reduced Oct-1 DNA binding 
      activity and to rescue of HLA-DRA inducibility. However, in the case of one 
      non-small cell lung carcinoma line (NSCLC), Rb re-expression failed to rescue 
      HLA-DRA inducibility despite successful re-establishment of Rb-function. We now 
      report that this failure is traceable to the failure of Rb to rescue normal Oct-1 
      function. Furthermore, histone deacetylase inhibitor treatment allows a bypass of 
      the Rb requirement and facilitates the MHC class II induction in this NSCLC line.
FAU - Osborne, Aaron R
AU  - Osborne AR
AD  - Department of Biochemistry and Molecular Biology, University of South Florida 
      College of Medicine, MDC Box 7, 12901 Bruce B. Downs Boulevard, Tampa, FL 33612, 
      USA.
FAU - Zhang, Hongquan
AU  - Zhang H
FAU - Blanck, George
AU  - Blanck G
LA  - eng
GR  - R01 CA81497/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20050414
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (HLA-DR alpha-Chains)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (Histone Deacetylase Inhibitors)
RN  - 0 (Octamer Transcription Factor-1)
RN  - 0 (Retinoblastoma Protein)
SB  - IM
MH  - Carcinoma, Non-Small-Cell Lung/*pathology
MH  - Cell Line
MH  - Cell Line, Tumor
MH  - DNA-Binding Proteins/metabolism
MH  - Enzyme Inhibitors/pharmacology
MH  - *Gene Expression Regulation
MH  - HLA-DR Antigens/genetics
MH  - HLA-DR alpha-Chains
MH  - Histocompatibility Antigens Class II/*genetics
MH  - Histone Deacetylase Inhibitors
MH  - Humans
MH  - Octamer Transcription Factor-1/*metabolism
MH  - Retinoblastoma Protein/*genetics
EDAT- 2005/12/20 09:00
MHDA- 2006/03/22 09:00
CRDT- 2005/12/20 09:00
PHST- 2005/01/06 00:00 [received]
PHST- 2005/12/20 09:00 [pubmed]
PHST- 2006/03/22 09:00 [medline]
PHST- 2005/12/20 09:00 [entrez]
AID - S0161-5890(05)00122-7 [pii]
AID - 10.1016/j.molimm.2005.03.013 [doi]
PST - ppublish
SO  - Mol Immunol. 2006 Feb;43(6):710-6. doi: 10.1016/j.molimm.2005.03.013. Epub 2005 
      Apr 14.