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Int J Med Sci. 2012;9(3):216-24. doi: 10.7150/ijms.4004. Epub 2012 Mar 7.

Effects of STAT3 gene silencing and rapamycin on apoptosis in hepatocarcinoma cells.

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  • 1Department of Hepatobiliary and Pancreatic Surgery, the First Hospital of Jilin University, Changchun, 130021, P. R. China.

Abstract

The PI3K/Akt/mTOR and JAK/STAT3 signaling pathways are important for regulating apoptosis, and are frequently activated in cancers. In this study, we targeted STAT3 and mTOR in human hepatocellular carcinoma Bel-7402 cells and examined the subsequent alterations in cellular apoptosis. The expression of STAT3 was silenced with small interfering RNA (siRNA)-expressing plasmid. The activity of mTOR was inhibited using rapamycin. Following treatment, Annexin V/propidium iodide staining followed by flow cytometry and Hoechst33258 immunofluorescence staining was used to examine cellular apoptosis. JC-1 staining was used to monitor depolarization of mitochondrial membrane (ΔΨm). Furthermore, the expression of activated caspase 3 protein was analyzed by Western blotting. Compared to non-treated or control siRNA-transfected cells, significantly higher levels of apoptosis were detected in siSTAT3-transfected or rapamycin-treated cells (P < 0.05), which was further enhanced in cells targeted for both molecules (P < 0.05). The pro-apoptotic effects were accompanied with concomitant depolarization of mitochondrial membrane and up-regulation of activated caspase 3. Combined treatments using rapamycin and STAT3 gene silencing significantly increases apoptosis in Bel-7402 cells, displaying more dramatic effect than any single treatment. This study provides evidence for targeting multiple molecules in cancer therapy.

KEYWORDS:

RNAi; STAT3; apoptosis; hepatocelluar carcinoma.; mTOR; rapamycin

PMID:
22408571
[PubMed - indexed for MEDLINE]
PMCID:
PMC3298013
Free PMC Article
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