Effects of 17‑DMAG on diffuse large B‑cell lymphoma cell apoptosis
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- Published online on: August 22, 2017 https://doi.org/10.3892/etm.2017.4995
- Pages: 3727-3731
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Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
17‑dimethylaminoethylamino‑17‑demethoxygeldanamycin (17‑DMAG) is a water soluble, semisynthetic derivative of endotoxin that has anticancer effects. The aim of the present study was to determine whether 17‑DMAG enhances the apoptosis of lymphoma cells in diffuse large B‑cell lymphoma. Apoptosis was induced in SU‑DHL‑4 diffuse large B‑cell lymphoma cells treated with 17‑DMAG, as evaluated by MTT assay and flow cytometry analysis. Apoptosis‑associated protein levels were assessed using western blotting, and the results indicated that B‑cell lymphoma 2 (Bcl‑2)‑associated protein X (Bax) was upregulated, whereas heat shock protein family A member 5 (HSPA5) and Bcl‑2 were downregulated. Additionally, staining with 5,5',6,6'‑Tetrachloro‑1,1',3,3'‑tetraethyl‑imidacarbocyanine iodide revealed that treatment with 17‑DMAG decreased mitochondrial membrane potential in SU‑DHL‑4 diffuse large B‑cell lymphoma cells. These results suggested that 17‑DMAG is able to inhibit proliferation in diffuse large B‑cell lymphoma cells in a concentration‑dependent manner. The underlying mechanism may be that 17‑DMAG induces oxidative stress, which inhibits the expression of HSPA5 and Bcl‑2 and promotes the expression of Bax, leading to the apoptosis of SU‑DHL‑4 cells. Taken together, these results indicated that 17‑DMAG may be an effective novel agent for the treatment of diffuse large B‑cell lymphoma.