Targeted cytotoxic somatostatin analog AN-162 inhibits growth of human colon carcinomas and increases sensitivity of doxorubicin resistant murine leukemia cells

Florian Hohla, Stefan Buchholz, Andrew V. Schally, Awtar K. Ganju-Krishan, Ferenc G. Rick, Luca Szalontay, Andrea Papadia, Gabor Halmos, Frank Koster, Elmar Aigner, Christian Datz, Stephan Seitz

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

The effect of the targeted cytotoxic somatostatin (SST) analog AN-162, consisting of doxorubicin (DOX) conjugated to SST carrier RC-121, was investigated on the growth of human colorectal cancer (CRC) cell lines HT-29, HCT-15, and HCT-116 and a DOX-resistant mouse leukemia cell line P388/R84. mRNA for SST-receptors and high affinity binding sites for SST were detected in all CRC cell lines and in P388/R84 cells. In contrast to DOX alone, AN-162 blocked HCT-116 cells and P388/R84 cells in S/G2 phase and increased the number of apoptotic cells. In vivo, AN-162 reduced the volume of CRC xenografts more effectively than its unconjugated components. Our results suggest that AN-162 inhibits growth of experimental CRC more effectively than DOX and increases sensitivity of DOX resistant human leukemia cells.

Original languageEnglish (US)
Pages (from-to)35-42
Number of pages8
JournalCancer letters
Volume294
Issue number1
DOIs
StatePublished - Aug 1 2010

Keywords

  • AN-162
  • Colon cancer
  • Doxorubicin
  • Somatostatin
  • Targeted therapy

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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