Purpose: To investigate the effect of isoliquiritigenin (ISL) on diffuse large B-cell lymphoma (DLBCL) cells and its underlying mechanism of action.Methods: The DLBCL cell line OCI-Ly19 was used in this study. Cell proliferation was measured by MTT assay. Apoptosis was evaluated using flow cytometry. Phosphorylation of Akt and mTOR was assessed using Western blotting.Results: DLBCL cell proliferation was suppressed by ISL in a concentration-dependent manner. The number of apoptotic cells increased following ISL treatment in a concentration-dependent manner (p < 0.05). ISL treatment also stopped the cell cycle at the G1 phase in a concentration-dependent manner. Western blot analysis indicated that there was no significant Akt and mTOR expression in cells treated with 10, 20, or 50 μM ISL (p < 0.05). However, Akt and mTOR phosphorylation was upregulated following treatment with 10, 20, or 50 μM ISL in a concentration-dependent manner (p < 0.05).Conclusion: The results demonstrate that ISL inhibits DLBCL cell proliferation and promotes cell apoptosis by blocking the cell cycle transition from the G1 to S phase, which is mediated by the inactivation of the Akt/mTOR signaling pathway.
Keywords: Isoliquiritigenin, Cell survival, Diffuse large B-cell lymphoma, Akt/mTOR signaling pathway
miR‑101 regulates the cell proliferation and apoptosis in diffuse large B‑cell lymphoma by targeting MEK1 via regulation of the ERK/MAPK signaling pathway