RGD Reference Report - Modulation of apoptosis, tumorigenesity and metastatic potential with antisense H-ras oligodeoxynucleotides in a high metastatic tumor model of hepatoma: LCI-D20.

General

Modulation of apoptosis, tumorigenesity and metastatic potential with antisense H-ras oligodeoxynucleotides in a high metastatic tumor model of hepatoma: LCI-D20.
Authors:	Liao, Y Tang, Z Y Ye, S L Liu, K D Sun, F X Huang, Z
Citation:	Liao Y, etal., Hepatogastroenterology. 2000 Mar-Apr;47(32):365-70.
RGD ID:	14688055
Pubmed:	PMID:10791191 (View Abstract at PubMed)
BACKGROUND/AIMS: To investigate the effect of antisense H-ras DNA on tumorigenesity, apoptosis and metastasis of a high metastatic tumor model of human hepatocellular carcinoma in nude mice LCI-D20. METHODOLOGY: LCI-D20 cells in primary culture were treated with 10 microns/L antisense oligodeoxynucleotide (ODN) drugs in vitro. 1.5 x 10(6) LCI-D20 cells with or without pretreatment were inoculated into each elevated subcutaneous (s.c.) flap in 14 nude mice, 6 animals for antisense H-ras oligodeoxynucleotide treated cells, 4 for H-ras non-specific antisense oligodeoxynucleotide treated cells, and the rest 4 for cells without pretreatment. RESULTS: In in vitro cell culture study, 5-day continuous suppression of H-ras expression by antisense H-ras oligodeoxynucleotide resulted in significant inhibition of the proliferation of LCI-D20 cells (t = 31.529, P < 0.01). In situ end-labeling detection showed that apoptotic cell death was significantly increased in cells with 5-day treatment of antisense H-ras oligodeoxynucleotide (34.0 +/- 4.5%) in comparing with cells without treatment (2.5 +/- 1.2%, t = 13.434, P < 0.01) or treated with non-specific antisense oligodeoxynucleotide (4.8 +/- 1.4%, t = 12.453, P < 0.01) at the corresponding time. In the in vivo experiment, at week 6, no palpable tumor could be found in 50% (3/6) of animals receiving cells with pretreatment of antisense H-ras oligodeoxynucleotide, while 100% (4/4, 4/4) of animals in the 2 control groups developed palpable tumors. Tumor growth in antisense H-ras treated animals was significantly retarded in comparison with that of the untreated (t = 3.509, P < 0.01) or non-specific antisense oligodeoxynucleotide treated animals (t = 3.452, P < 0.01). 75% to 100% of animals in the 2 control groups developed lung metastases, while in antisense H-ras treated animals lung metastasis foci could not be found by random serial section and microscopy (u = 2.536, P < 0.01; u = 3.162, P < 0.01, respectively). CONCLUSIONS: Specific inhibition of H-ras expression by antisense H-ras oligodeoxynucleotides could not only induce apoptotic cell death, inhibit the growth rate of LCI-D20 cells in vitro and in vivo, but also alter in vivo tumorigenesity and metastatic potential of LCI-D20 cells.

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Term	Qualifier	Evidence	With	Reference	Notes	Source	Original Reference(s)
hepatocellular carcinoma	treatment	IMP		14688055	human cells in a mouse model	RGD
hepatocellular carcinoma	treatment	ISO	HRAS (Homo sapiens)	14688055; 14688055	human cells in a mouse model	RGD

Objects Annotated

Genes (Rattus norvegicus)

Hras (HRas proto-oncogene, GTPase)

Genes (Mus musculus)

Hras (Harvey rat sarcoma virus oncogene)

Genes (Homo sapiens)

HRAS (HRas proto-oncogene, GTPase)

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Modulation of apoptosis, tumorigenesity and metastatic potential with antisense H-ras oligodeoxynucleotides in a high metastatic tumor model of hepatoma: LCI-D20.