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 Krishan; Ferenc G. Rick; Luca Szalontay; Andrea Papadia; Gabor Halmos; Frank Koster; Elmar Aigner; Christian Datz; Stephan Seitz

doi:10.1016/j.canlet.2010.01.018

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 Krishan, Ferenc G. Rick, Luca Szalontay, Andrea Papadia, Gabor Halmos, Frank Koster, Elmar Aigner, Christian Datz, Stephan Seitz

^*Corresponding author for this work

Clinic of Gynecology and Obstetrics

14 Citations (Scopus)

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 language	English
Journal	Cancer Letters
Volume	294
Issue number	1
Pages (from-to)	35-42
Number of pages	8
ISSN	0304-3835
DOIs	https://doi.org/10.1016/j.canlet.2010.01.018
Publication status	Published - 01.08.2010

Research Areas and Centers

Research Area: Luebeck Integrated Oncology Network (LION)

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This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.canlet.2010.01.018

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Hohla, F., Buchholz, S., Schally, A. V., Krishan, A., Rick, F. G., Szalontay, L., Papadia, A., Halmos, G., Koster, F., Aigner, E., Datz, C., & Seitz, S. (2010). Targeted cytotoxic somatostatin analog AN-162 inhibits growth of human colon carcinomas and increases sensitivity of doxorubicin resistant murine leukemia cells. Cancer Letters, 294(1), 35-42. https://doi.org/10.1016/j.canlet.2010.01.018

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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.",

author = "Florian Hohla and Stefan Buchholz and Schally, {Andrew V.} and Awtar Krishan and Rick, {Ferenc G.} and Luca Szalontay and Andrea Papadia and Gabor Halmos and Frank Koster and Elmar Aigner and Christian Datz and Stephan Seitz",

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Hohla, F, Buchholz, S, Schally, AV, Krishan, A, Rick, FG, Szalontay, L, Papadia, A, Halmos, G, Koster, F, Aigner, E, Datz, C & Seitz, S 2010, 'Targeted cytotoxic somatostatin analog AN-162 inhibits growth of human colon carcinomas and increases sensitivity of doxorubicin resistant murine leukemia cells', Cancer Letters, vol. 294, no. 1, pp. 35-42. https://doi.org/10.1016/j.canlet.2010.01.018

TY - JOUR

T1 - Targeted cytotoxic somatostatin analog AN-162 inhibits growth of human colon carcinomas and increases sensitivity of doxorubicin resistant murine leukemia cells

AU - Hohla, Florian

AU - Buchholz, Stefan

AU - Schally, Andrew V.

AU - Krishan, Awtar

AU - Rick, Ferenc G.

AU - Szalontay, Luca

AU - Papadia, Andrea

AU - Halmos, Gabor

AU - Koster, Frank

AU - Aigner, Elmar

AU - Datz, Christian

AU - Seitz, Stephan

PY - 2010/8/1

Y1 - 2010/8/1

N2 - 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.

AB - 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.

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SN - 0304-3835

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JO - Cancer Letters

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

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