Fig. 3: Silencing BCL11B enhanced chemosensitivity and induced cell differentiation in HCC. | Cell Death & Disease

Fig. 3: Silencing BCL11B enhanced chemosensitivity and induced cell differentiation in HCC.

From: BCL11B suppresses tumor progression and stem cell traits in hepatocellular carcinoma by restoring p53 signaling activity

Fig. 3

a BCL11B silencing resulted in lower percentages of apoptosis rate under 5 μM sorafenib or 2 μM doxorubicin treatment, while BCL11B overexpression led to higher percentages of apoptosis rate under 5 μM sorafenib or 2 μM doxorubicin treatment, compared with corresponding control cells, respectively. b Clone formation assays showed that BCL11B silencing resulted in higher numbers of clone under 5 μM sorafenib or 2 μM doxorubicin treatment, while BCL11B overexpression decreased number of Huh7 clone under 5 μM sorafenib or 2 μM doxorubicin treatment. c–e Dynamic changes of the protein expression levels of CSC markers (EpCAM and CD24) and mature hepatocyte markers (CK8 and GP6C) due to BCL11B expression manipulations in MHCC97L cells (c), HepG2 (d), and Huh7 cells (e). f Alterations of the percentage of CD24+ and CK8+ cells in indicated HCC cells due to BCL11B expression manipulations were evaluated by flow cytometry. g Immunofluorescence analysis of CD24 and CK8 expression in BCL11B-knockdown MHCC97L cells and HepG2 cells, as well as BCL11B-overexpressing Huh7 cells, with their corresponding parental cells as controls, respectively. Scale bar: 10 μm. Means ± SD from three independent experiments are presented; *P < 0.05; **P < 0.01; ***P < 0.001.

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