| Literature DB >> 29969367 |
Xinyao Li1,2,3, Zhengchang He1,2,3, Bingqing Cheng4,2,3, Qin Fang4,5, Dan Ma1,2,3, Tingting Lu1,2,3, Danna Wei1,2,3, Xingyi Kuang1,2,3, Sishi Tang1,2,3, Jie Xiong1,2,3, Jishi Wang1,2,3.
Abstract
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-κB 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-κB 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.Entities:
Keywords: BCLAF1; HDAC4; LMK-235; NF-kB; apoptosis; diffuse large B cell lymphoma
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Year: 2018 PMID： 29969367 PMCID： PMC6154843 DOI： 10.1080/15384047.2018.1472188
Source DB: PubMed Journal: Cancer Biol Ther ISSN： 1538-4047 Impact factor: 4.742