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Aberrant expression of BCL 11 B in mycosis fungoides and its potential role in interferon‐induced apoptosis
Author(s) -
Gu Xiaoguang,
Wang Yang,
Zhang Gaolei,
Li Weiwei,
Tu Ping
Publication year - 2013
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/1346-8138.12160
Subject(s) - mycosis fungoides , apoptosis , cancer research , downregulation and upregulation , biology , interferon , immunology , lymphoma , gene , biochemistry
BCL 11 B is a K ruppel‐like C 2 H 2‐type zinc finger transcription factor, which has been associated with several human malignancies. Recent evidence showed that overexpressed BCL 11 B conferred chemoresistance to malignant T cells and that inhibiting BCL 11 B led to increased apoptosis, suggesting its potential pathogenic relevance in cutaneous T ‐cell lymphomas ( CTCL ), which were characterized by the resistance to chemotherapy‐induced apoptosis. To investigate the expression pattern of BCL 11 B in different stages of mycosis fungoides ( MF ), quantitative reverse transcription polymerase chain reaction and immunohistochemistry were performed to compare the m RNA and protein expression among different stages of MF and benign inflammatory dermatoses ( BID ), respectively. BCL 11 B demonstrated significant upregulation in all stages of MF, compared with BID , in both m RNA expression level and protein level. In addition, BCL 11 B expression increased with advancing lesion tumor stage and overall disease stage. Further, to evaluate the dynamic expression of BCL11B under CTCL ‐directed treatment, BCL11B expression and cell apoptosis were evaluated after interferon (IFN)‐α‐2b and methotrexate treatment on CTCL cell line H ut78 cells. IFN ‐α‐2b, but not methotrexate, induced BCL11B inhibition and cell apoptosis, suggesting that BCL11B may play important roles in the anti‐ CTCL effect of IFN ‐α‐2b. In conclusion, our study demonstrated the overexpression of BCL11B in MF lesions and its potential relevance to disease progression. In addition, we provided evidence for BCL 11 B inhibitory approaches as a potential treatment to target chemoresistant tumor cells in advanced MF .