Objective      To explore the growth inhibition mechanism of hepatocellular carcinoma HCC cells through comparing their responses to sodium arsenite

CD13 and CD133 expressions

and formation of tumor spheres in HepG2

Hep3B

HuH7 and SMCC-7721 cells

and analyze Oct4 and Sox2 gene expression in HuH7 and primary HCC cells treated with low concentration of sodium arsenite.       Methods      CCK-8 assay was used to measure the effect of different concentrations (0.1

0.2

0.4

0.6

0.8 and 1.0 μg/mL) of sodium arsenite on growth inhibition of HepG2

Hep3B

HuH7 and SMCC-7721 cells for 48

72 and 96 h

respectively. The expression of CD13 and CD133 in HepG2

Hep3B

HuH7

SMCC-7721 and primary HCC cells and the formation of tumor spheres were analyzed to determine liver cancer stem cells (LCSCs). The expression of Oct4 and Sox2 detected in HuH7 and primary HCC cells treated with 0.5 μg/mL of sodium arsenite

and the effect of low concentration of sodium arsenite on LCSCs was analyzed.       Results      In 48

72 and 96 h after treatment with sodium arsenite

the growth of HepG2

Hep3B

HuH7 and SMCC-7721 cells was inhibited

and the inhibitory effect of sodium arsenite on HCC cells was associated with the treating time and concentration. In 96 h

0.2 and 0.4 μg/mL of sodium arsenite significantly inhibited the growth of SMCC-7721 cells (P0.05

P0.01)

and 0.4 μg/mL of sodium arsenite markedly inhibited the proliferation of HepG2 cells (P0.01) and Hep3B cells (P0.01). In addition

0.8 μg/mL of sodium arsenite exhibited highly significant growth inhibitory effect on HuH7 cells (P0.01)

while 0.1 to 0.6 μg/mL of sodium arsenite promoted the proliferation of HuH7 cells

but the differences were not statistically significant (P0.05). However

low concentration of sodium arsenite did not promote the proliferation of HepG2

Hep3B and SMCC-7721 cells. SMCC-7721

HepG2 and Hep3B cells had no CD133 expression and no format

ion of tumor spheres. In contrast

HuH7 and primary HCC cells expressed CD133 and CD13

and formed typical tumor spheres. HuH7 and primary HCC cells contained CD133

+

CD13

+

LCSCs and expressed Oct4 and Sox2 gene and protein

and 0.5 μg/mL of sodium arsenite could down-regulate the expression.       Conclusion      Low concentration of sodium arsenite down-regulates or inhibits Oct4 and Sox2 at transcription and protein levels in HuH7 and primary HCC cells containing CD133

+

CD13

+

LCSCs

which suggests that low concentration of sodium arsenite may induce differentiation of CD133

+

CD13

+

LCSCs.