Table 1 GAL1 protects HepG2 HCC cells from DOX-and sorafenib-induced cell death in vitro.

From: Galectin-1 confers resistance to doxorubicin in hepatocellular carcinoma cells through modulation of P-glycoprotein expression

 

DOX IC50 (µM) (CI95)

Sorafenib IC50 (µM) (CI95)

48 h

72 h

24 h

HepG2

1.13 (0.77–1.67)

0.86 (0.67–1.12)

17.18 (15.00–19.66)

HepG2-M

1.19 (0.89–1.59)

0.81 (0.69–0.96)

13.36 (11.79–15.13)

HepG2-GAL1

1.97 (1.58–2.47) (165%*)

1.31 (1.17–1.46) (162%*)

32.25 (22.31–46.61) (241%*)

HepG2-shScr

1.33 (1.04–1.72)

0.97 (0.78–1.21)

nd

HepG2-shGAL1

0.84 (0.55–1.29) (63%#)

0.44 (0.33–0.6) (45%#)

nd

  1. HepG2 cells with different levels of GAL1 expression were cultured in the presence of increasing concentrations of DOX (0–5 µM) or sorafenib (5–100 µM) for the indicated times. Percentages of cell viability were assessed by MTT assay and plotted versus DOX or sorafenib concentration on dose–response curves for each time. DOX or sorafenib half-maximal inhibitory concentration (IC50) values were obtained from dose–response viability curves for each cell line and incubation time (Fig. 1B, D) using the statistical program GraphPad Prism for Windows, version 6.01. *, #, with respect to IC50 values obtained for HepG2-M and HepG2-shScr cells, respectively.
  2. CI95 95% confidence interval; nd not determined.
Back to article page