Inhibition of the PI3K/AKT signaling pathway sensitizes diffuse large B-cell lymphoma cells to treatment with proteasome inhibitors via suppression of BAG3.
Inhibition of the PI3K/AKT signaling pathway sensitizes diffuse large B-cell lymphoma cells to treatment with proteasome inhibitors via suppression of BAG3.
Oncol Lett. 2019 Apr;17(4):3719-3726
Authors: Yuan T, Zhang F, Zhou X, Li Y, Zhang Y, Xu Y, Wang X
Abstract
Proteasome inhibitors represent a novel class of drugs that have clinical efficacy against hematological and solid cancer types, including acute myeloid leukaemia, myelodysplastic syndrome an non-small cell lung cancer. It has been demonstrated that the anti-apoptotic protein B-cell lymphoma-2-associated athanogene 3 (BAG3) is induced by proteasome inhibitors in various cancer cells and serves an important role in chemotherapy resistance. The phosphatidylinositol 3-kinase (PI3K)/RAC-α serine/threonine-protein kinase (AKT) pathway is constitutively activated in a number of lymphoid malignancy types, including diffuse large B-cell lymphoma (DLBCL) and Burkitt lymphoma. In the present study, the aim was to elucidate the role of the PI3K/AKT signaling pathway in the induction of BAG3, following exposure to a proteasome inhibitor in DLBCL cell lines. Bortezomib and MG132 were used as proteasome inhibitors. Western blotting was used to evaluate the roles of proteasome inhibitors and the PI3K/AKT pathway in BAG3 induction in DLBCL cells (LY1 and LY8), and LY294002 was used to block the PI3K/AKT pathway. Cell viability was detected using a Cell Counting Kit-8 assay. Apoptosis of L...
Source: Oncology Letters - Category: Cancer & Oncology Tags: Oncol Lett Source Type: research
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