In this study, we detected the expression of FACL4
mRNA in 40 patients with hepatic
carcinoma and its adjacent normal tissues by semi-quantitative RT-PCR. The changes of proliferation and apoptosis of
hepatic cancer cell line HepG2 with FACL4
protein expression were examined by MTT and flow cytometry respectively after FACL4 selective inhibitor
triacsin C treatment. The activity related to apoptosis of
proteinases,
caspase-3,
caspase-8 and
caspase-9, were detected by colorimetry. The expression related to apoptosis of
protein, wt-p53, Bax and Bcl-2, in HepG2 cells were evaluated by S-P immunocytochemical dyeing. The results were: (1) FACL4
mRNA was expressed in 95.0% of
hepatic cancer tissue, while the positive expression of FACL4
mRNA was 82.5% in
cancer adjacent normal liver tissues. Moreover, there was a statistically significant increased in quantity of FACL4
mRNA in
cancer tissues compared with adjacent normal liver tissues. (2) The concentration of
triacsin C (0.5-2 mg/L) could inhibit the proliferation and induce the apoptosis of HepG2 cells significantly in a dose- and time-effect. (3) During the apoptosis of HepG2 cells induced by
triacsin C, flow cytometry coupled with
Rhodamine 123 dyeing showed that mitochondrial transmembrane potential of HepG2 declined significantly, and the activity of
caspase-9 and
caspase-3 increased more remarkably than
caspase-8. Besides, the increased apoptosis was accompanied by increased Bax, and decreased wtp53 and Bcl-2
protein levels. The present study suggested that FACL4 might play a role in the growth of
hepatic cancer cells. FACL4 selective inhibitor
triacsin C leads to a marked growth inhibition of human liver
tumor cells, based on the inhibition of proliferation and induction of apoptosis. The apoptotic process was mediated by intrinsic mitochondrial apoptotic pathway due to activation of
caspase-9 and
caspase-3. The increased apoptosis was accompanied by upregulation of Bax, and decreased wt-p53 and Bcl-2
protein level.