Fig 2: SiRNA-mediated knockdown of BCL2 family members in ALCL cell lines. Life cell imaging shows effects of knockdown of BCL2 family members on growth (cell counts) and apoptosis (caspase 3/7 activity) 48 h after onset of treatment with siRNA oligos. (a) Knockdown of MCL1 and BCLXL; (b) knockdown of MCL1 and BCL2A1. Note synergistic effects of MCL1 and BCLXL knockdown in cell line L-82 and additive effects of MCL1 and BCL2A1 knockdown in cell line SU-DHL-1. The horizontal line shows the expected additive effects of the combination of siRNA oligos.

Fig 3: Identifying a novel lncRNA PANTR1/miR-587/BCL2A1 axis in HCC progression. (a) HepG2 and Hep3B cells were transfected with OE-NC, OE-PANTR1, OE-PANTR1+Sh-NC, and OE-PANTR1+Sh-BCL2A1 as indicated, and transfection efficiencies were detected by qRT-PCR. (b, c) Cell proliferation abilities of pretreated HepG2 and Hep3B cells were detected by CCK-8 assays. (d, e) Flow cytometer assay was applied to evaluate the cell apoptosis rate of pretreated HepG2 and Hep3B cells. (f, g) Transwell migration assays were conducted to evaluate the migration level of pretreated HepG2 and Hep3B cells, and cell migration numbers were accounted. Comparative statistics are shown. Scale bars: 20 µm. (h–j) The Warburg effect phenomenon-related lactate production (h), glycolysis rates (i), and ATP levels (j) in HCC cells were measured. Data are shown as the mean ± standard deviation (n = 3). *P < 0.05 and **P < 0.01.

Fig 4: Drug sensitivity analysis of five central protein-coding genes. (A) Regulatory pathway map of BCL2A1 and the sensitive target of Vemurafenib. (B) The scatter plot shows the sensitivity analysis of BCL2A1 and the antitumor drug Vemurafenib. (C) Box-plot show the molecular formula of the Vemurafenib and the expression levels of BCL2A1 were analyzed using RNA sequencing data from 24 no drug and 54 with drug subjects in the GSE97681. (D) The expression levels of PI3K, AKT, P-Akt and BCL2A1 in MCF7, MDA-MB-231, SKBR3 and MCF10A cells were detected by Western Blot. (E) Vemurafenib inhibited cell viability in breast cancer cells. The concentration of vemurafenib resulting in 50% inhibition of control growth (IC50) was calculated. (F) Vemurafenib inhibit cell viability at different times. Vemurafenib (0, 20, 40, 60µM) inhibited MCF-7, SKBR3 and MDA-MB-231 cell viability at 0, 24, 48, and 72h. *P<0.05, **P<0.01, ***P<0.001.

Fig 5: Inhibitory effect of Vemurafenib on different breast cancer cell lines. (A) Vemurafenib suppressed PI3K, AKT, p-AKT and BCL2A1 expression in MDA-MB-231cells. (B) Vemurafenib suppressed PI3K, AKT, p-AKT and BCL2A1 expression in MCF-7 cells. (C) Vemurafenib suppressed PI3K, AKT, p-AKT and BCL2A1 expression in SKBR3 cells. (D) Decreased levels of BCL2A1 in MDA-MB-231 cells treated with different concentrations of vemurafenib (0, 20, 40, 60 µM) were determined by RT-qPCR. (E) Decreased levels of BCL2A1 in MCF-7 cells treated with different concentrations of vemurafenib (0, 20, 40, 60 µM) were determined by RT-qPCR. (F) Decreased levels of BCL2A1 in SKBR3 cells treated with different concentrations of vemurafenib (0, 20, 40, 60 µM) were determined by RT-qPCR. (*P<0.05, **P<0.01, ***P<0.001.).