%0 Journal Article
%T Effect of BCLAF1 on HDAC inhibitor LMK-235-mediated apoptosis of diffuse large B cell lymphoma cells and its mechanism
%A Bingqing Cheng
%A Dan Ma
%A Danna Wei
%A Jie Xiong
%A Jishi Wang
%A Qin Fang
%A Sishi Tang
%A Tingting Lu
%A Xingyi Kuang
%A Xinyao Li
%A Zhengchang He
%J Archive of "Cancer Biology & Therapy".
%D 2018
%R 10.1080/15384047.2018.1472188
%X Diffuse large B-cell lymphoma (DLBCL) is the most common type of adult lymphoma. It is a group of malignant tumors with a large number of clinical manifestations and prognoses. Therefore, it is necessary to explore its unknown potential therapeutic targets. Histone deacetylase inhibitor (HDACi) is a novel drug for the treatment of DLBCL, however pan-HDACis cannot be ignored because of their clinical efficacy. By contrast, specific HDACi is well-tolerated, and LMK-235 is a novel HDACi that is a specific inhibitor of HDAC4 and HDAC5. In this study, we investigated the up-regulation of BCLAF1 through NF-¦ĘB signaling pathways in LMK-235, mediating the apoptosis of two diffuse large B-cell lymphoma cell lines, OCI-LY10 and OCI-LY3. Further studies showed that BCLAF1 expression was increased in DLBCL cells after treatment with the NF-¦ĘB inhibitor Bay11-7082. The combination of Bay11-7082 and siRNA si-HDAC4 significantly increased BCLAF1 expression and further increased apoptosis. These results indicate that BCLAF1 plays an important role in LMK-235-mediated apoptosis and may be a potential target for the treatment of diffuse large B-cell lymphoma
%K LMK-235
%K BCLAF1
%K HDAC4
%K NF-kB
%K apoptosis
%K diffuse large B cell lymphoma
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6154843/