Reference - Detail
| RRC ID | 41613 |
|---|---|
| Author | Yazawa T, Ito T, Kamma H, Suzuki T, Okudela K, Hayashi H, Horiguchi H, Ogata T, Mitsui H, Ikeda M, Kitamura H. |
| Title | Complicated mechanisms of class II transactivator transcription deficiency in small cell lung cancer and neuroblastoma. |
| Journal | Am J Pathol |
| Abstract |
Small cell lung cancer (SCLC) and neuroblastoma (NB), the most aggressive adult and infant neuroendocrine cancers, respectively, are immunologically characterized by a severe reduction in major histocompatibility complex (MHC) that is indispensable for anti-tumor immunity. We had reported that the severe reduction of MHC in SCLC was caused by a deficient interferon (IFN)-gamma-inducible expression of class II transactivator (CIITA) that is known as a very important transcription factor for IFN-gamma-inducible class II and class I MHC expression (Yazawa T, Kamma H, Fujiwara M, Matsui M, Horiguchi H, Satoh H, Fujimoto M, Yokohama K, Ogata T: Lack of class II transactivator causes severe deficiency of HLA-DR expression in small cell lung cancer. J Pathol 1999, 187:191-199). Here, we demonstrate that the reduction of MHC in NB was also caused by a deficient IFN-gamma-inducible expression of CIITA and that the deficiency in SCLC and NB was caused by similar mechanisms. Human achaete-scute complex homologue (HASH)-1, L-myc, and N-myc, which are specifically overexpressed in SCLC and NB, bound to the E-box in CIITA promoter IV and reduced the transcriptional activity. Anti-sense oligonucleotide experiments revealed that overexpressed L-myc and N-myc lie upstream in the regulatory pathway of HASH-1 expression. The expression of HASH-1 was also up-regulated by IFN-gamma. Our results suggest that SCLC and NB have complicated mechanisms of IFN-gamma-inducible CIITA transcription deficiency through the overexpressed HASH-1, L-myc, and N-myc. These complicated mechanisms may play an important role in the escape from anti-tumor immunity. |
| Volume | 161(1) |
| Pages | 291-300 |
| Published | 2002-7-1 |
| DOI | 10.1016/S0002-9440(10)64181-8 |
| PII | S0002-9440(10)64181-8 |
| PMID | 12107114 |
| PMC | PMC1850684 |
| MeSH | Basic Helix-Loop-Helix Transcription Factors Carcinoma, Small Cell / genetics* Carcinoma, Small Cell / immunology Carcinoma, Small Cell / metabolism DNA-Binding Proteins / metabolism DNA-Binding Proteins / pharmacology Humans Interferon-gamma / pharmacology Lung Neoplasms / genetics* Lung Neoplasms / immunology Lung Neoplasms / metabolism Major Histocompatibility Complex / immunology Neuroblastoma / genetics* Neuroblastoma / immunology Neuroblastoma / metabolism Nuclear Proteins* Proto-Oncogene Proteins c-myc / metabolism Proto-Oncogene Proteins c-myc / pharmacology Trans-Activators / genetics* Transcription Factors / metabolism Transcription Factors / pharmacology Transcription, Genetic* / drug effects Tumor Cells, Cultured / drug effects |
| IF | 3.491 |
| Times Cited | 31 |
| WOS Category | PATHOLOGY |
| Altmetric score |
オルトメトリクス指標項目
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| The most frequently cited source | Patent(IFI CLAIMS) |
| Total number of mentions | 2 |
| Altmetric score changes over past 6months | 0.0 |
| Resource | |
| Human and Animal Cells | HeLa(RCB0007) |