Page 63 - Haematologica March 2020

Genetic and epigenetic regulation of latexin transcription
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Figure 3. HMGB2 knockdown increases apoptosis and decreases proliferation. (A) HMGB2 knockdown increases apoptosis of EML cells. Representative FACS plots (left) and quantification (right) of Annexin V+ and 7AAD- apoptotic EML cells transduced with control-shRNA (Con) or HMGB2 knockdown shRNA lentivirus (HMGB2 KD). (B) HMGB2 knockdown increases the percentage of active caspase 3 positive EML cells. Representative flow cytometry profile (left) and quantification (right) of active caspase 3 immnuofluorescence signal in EML cells. (C) HMGB2 knockdown decreases proliferation of EML cells. Representative FACS plots showing the G0/G1 (BrdU- and 7AAD-), S (BrdU+), and G2/M (BrdU- and 7AAD+) phages of cell cycle in EML cells (left). (Right) Frequencies of each phase. (D) Lxn knockdown (HMGB2 KD + Lxn KD) restores the percentage of apoptotic (Annexin V+) HMGB2-knockdown EML cells (HMGB2 KD) to a level comparable to control group (Con). (E) Lxn knockdown (HMGB2 KD + Lxn KD) restores the percentage of active caspase-3 positive HMGB2-knockdown EML cells (HMGB2 KD) to a level comparable to control group (Con). (F) Lxn knockdown (HMGB2 KD + Lxn KD) did not restore the cell cycle status of HMGB2-knockdown EML cells (HMGB2 KD) to control group level (Con). Data presented as the average±Standard Deviation of six measurements from two independent experiments. *P<0.05; **P<0.01; ***P<0.001.
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