Somatostatin analogue RC-160 inhibits the growth of transplanted colon cancer in rats

Y. Qin, Andrew V Schally, G. Willems

Research output: Contribution to journalArticle

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Abstract

The effect of somatostatin analogue RC-160 on the growth of DHD/K12 rat colon cancer has been investigated in vivo as well as in vitro. Twenty syngeneic BDIX rats with s.c. implanted tumors were divided randomly into 2 groups. The rats from each group received a daily s.c. injection of either RC-160 (100 μg/kg/day) or injection vehicle as control for 37 days starting from the day of tumor inoculation. Tumor volumes were measured every 3-4 days. At the end of the treatment, the mean tumor volume was 504.5 ± 97.0 mm3 in the control group and 177.8 ± 60.5 mm3 in the RC-160 treated group (p < 0.01). The tumor volume doubling time was calculated to be 11 days in the control group and 13.5 days in the RC-160 group, respectively. The tumor growth delay time was 18 days. Using bromodeoxyuridine labelling in vivo, the mean labelling index in the tumors was decreased by 35% (p < 0.01) after RC-160 treatment. Total protein and total DNA contents in the tumors were decreased by 70.1% (p < 0.05) and 68.7% (p < 0.05), respectively. The data indicate that somatostatin analogue RC-160 inhibits the growth of DHD/K12 colon cancer in vivo. In 2 studies in vitro, DHD/K12 cells were cultured for 72 hr with RC-160 and natural somatostatin-14 (S-S-14) at concentrations ranging from 62.5 ng/ml to 2,000 ng/ml. Tumor-cell growth was measured spectrophotometrically by the crystal violet staining assay. No direct effect on tumor cell growth in vitro was observed with either RC-160 or S-S-14, possibly because of the loss of somatostatin receptors in previous passages of the DHD/K12 cell line.

Original languageEnglish
Pages (from-to)765-770
Number of pages6
JournalInternational Journal of Cancer
Volume47
Issue number5
StatePublished - Jan 1 1991
Externally publishedYes

Fingerprint

Somatostatin
Colonic Neoplasms
Growth
Tumor Burden
Neoplasms
Gentian Violet
Somatostatin Receptors
Control Groups
Injections
vapreotide
Bromodeoxyuridine
Cultured Cells
Staining and Labeling
Cell Line
DNA
Therapeutics
In Vitro Techniques

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Somatostatin analogue RC-160 inhibits the growth of transplanted colon cancer in rats. / Qin, Y.; Schally, Andrew V; Willems, G.

In: International Journal of Cancer, Vol. 47, No. 5, 01.01.1991, p. 765-770.

Research output: Contribution to journalArticle

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abstract = "The effect of somatostatin analogue RC-160 on the growth of DHD/K12 rat colon cancer has been investigated in vivo as well as in vitro. Twenty syngeneic BDIX rats with s.c. implanted tumors were divided randomly into 2 groups. The rats from each group received a daily s.c. injection of either RC-160 (100 μg/kg/day) or injection vehicle as control for 37 days starting from the day of tumor inoculation. Tumor volumes were measured every 3-4 days. At the end of the treatment, the mean tumor volume was 504.5 ± 97.0 mm3 in the control group and 177.8 ± 60.5 mm3 in the RC-160 treated group (p < 0.01). The tumor volume doubling time was calculated to be 11 days in the control group and 13.5 days in the RC-160 group, respectively. The tumor growth delay time was 18 days. Using bromodeoxyuridine labelling in vivo, the mean labelling index in the tumors was decreased by 35{\%} (p < 0.01) after RC-160 treatment. Total protein and total DNA contents in the tumors were decreased by 70.1{\%} (p < 0.05) and 68.7{\%} (p < 0.05), respectively. The data indicate that somatostatin analogue RC-160 inhibits the growth of DHD/K12 colon cancer in vivo. In 2 studies in vitro, DHD/K12 cells were cultured for 72 hr with RC-160 and natural somatostatin-14 (S-S-14) at concentrations ranging from 62.5 ng/ml to 2,000 ng/ml. Tumor-cell growth was measured spectrophotometrically by the crystal violet staining assay. No direct effect on tumor cell growth in vitro was observed with either RC-160 or S-S-14, possibly because of the loss of somatostatin receptors in previous passages of the DHD/K12 cell line.",
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