Neurotensin stimulates growth of colon cancer

K. Yoshinaga; B. M. Evers; M. Izukura; D. Parekh; T. Uchida; C. M. Townsend; J. C. Thompson

doi:10.1016/0960-7404(92)90025-G

Neurotensin stimulates growth of colon cancer

K. Yoshinaga
, B. M. Evers
, M. Izukura
, D. Parekh
, T. Uchida
, C. M. Townsend
, J. C. Thompson

Producción científica: Article › revisión exhaustiva

51 Citas (Scopus)

Resumen

Neurotensin (NT), a peptide from the distal gut that is released by fat ingestion, stimulates the growth of normal small bowel and colonic mucosa. The purpose of this study was to determine whether chronic administration of NT would affect the growth of a mouse colon cancer (MC-26) and a human colon cancer (LoVo) in vivo. In experiment 1, male Balb/c mice were inoculated with MC-26 cells (5 × 10⁴) and then randomized to four treatment groups receiving either saline (control) or NT (150, 300 or 600 μg kg^-1) administered subcutaneously (s.c.) every 8 h for 21 days. In experiment 2, 60 mice with MC-26 tumours were randomized to receive saline (control) or NT (300 or 600 μg kg^-1) for 28 days, and survival was then assessed. In experiment 3, 16 athymic nude mice with LoVo tumour xenografts were randomized to receive either saline (control) or NT (600 μg kg^-1). We found that administration of NT (300 and 600 μg kg^-1) significantly stimulated mean tumour area, weight and DNA, RNA and protein content of MC-26 tumours. In addition, the survival rate of mice bearing MC-26 tumours and treated with either dose of NT was significantly decreased compared with the control group given saline injections. Similarly, NT (600 μg kg^-1) stimulated growth (tumour area, weight and nucleic acid contents) of the human colon cancer, LoVo. We conclude that NT acts as a trophic factor for the colon cancer cell lines MC-26 and LoVo in vivo. NT may play an important role in growth regulation of certain colon cancers.

Idioma original	English
Páginas (desde-hasta)	127-134
Número de páginas	8
Publicación	Surgical Oncology
Volumen	1
N.º	2
DOI	https://doi.org/10.1016/0960-7404(92)90025-G
Estado	Published - abr 1992

Nota bibliográfica

Funding Information:
This work was supported by grants from the National Institute of Health (5R37 DK 15241, PO1 DK 35608) and the American Cancer Society (PDT 220).

Funding Information:
*Visiting Scientist from the Second Department of Surgery, Tokyo Medical and Dental University, Tokyo, Japan. TRecipient of an American Surgical Association Foundation Fellowship Award and a UTMB Small Grant Award. *Visiting Scientist from the First Department of Surgery, Osaka University Medical School, Osaka, Japan. §Visiting Scientist from the University of Witwatersrand, Johannesburg, South Africa; supported by scholarships from the Michael and Janie Miller Foundation and the Medical Research Council, South Africa.

Financiación

This work was supported by grants from the National Institute of Health (5R37 DK 15241, PO1 DK 35608) and the American Cancer Society (PDT 220). *Visiting Scientist from the Second Department of Surgery, Tokyo Medical and Dental University, Tokyo, Japan. TRecipient of an American Surgical Association Foundation Fellowship Award and a UTMB Small Grant Award. *Visiting Scientist from the First Department of Surgery, Osaka University Medical School, Osaka, Japan. §Visiting Scientist from the University of Witwatersrand, Johannesburg, South Africa; supported by scholarships from the Michael and Janie Miller Foundation and the Medical Research Council, South Africa.

Financiadores	Número del financiador
Michael and Janie Miller Foundation
Italian National Health Institute	5R37 DK 15241, PO1 DK 35608
American Cancer Society	PDT 220
National Institute of Diabetes and Digestive and Kidney Diseases	P01DK035608
American Surgical Association Foundation
University of Texas Medical Branch at Galveston
University of the Witwatersrand, Johannesburg
Medical Research Council

ODS de las Naciones Unidas

Este resultado contribuye a los siguientes Objetivos de Desarrollo Sostenible

Good health and well being

ASJC Scopus subject areas

Surgery
Oncology

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title = "Neurotensin stimulates growth of colon cancer",

abstract = "Neurotensin (NT), a peptide from the distal gut that is released by fat ingestion, stimulates the growth of normal small bowel and colonic mucosa. The purpose of this study was to determine whether chronic administration of NT would affect the growth of a mouse colon cancer (MC-26) and a human colon cancer (LoVo) in vivo. In experiment 1, male Balb/c mice were inoculated with MC-26 cells (5 {\texttimes} 104) and then randomized to four treatment groups receiving either saline (control) or NT (150, 300 or 600 μg kg-1) administered subcutaneously (s.c.) every 8 h for 21 days. In experiment 2, 60 mice with MC-26 tumours were randomized to receive saline (control) or NT (300 or 600 μg kg-1) for 28 days, and survival was then assessed. In experiment 3, 16 athymic nude mice with LoVo tumour xenografts were randomized to receive either saline (control) or NT (600 μg kg-1). We found that administration of NT (300 and 600 μg kg-1) significantly stimulated mean tumour area, weight and DNA, RNA and protein content of MC-26 tumours. In addition, the survival rate of mice bearing MC-26 tumours and treated with either dose of NT was significantly decreased compared with the control group given saline injections. Similarly, NT (600 μg kg-1) stimulated growth (tumour area, weight and nucleic acid contents) of the human colon cancer, LoVo. We conclude that NT acts as a trophic factor for the colon cancer cell lines MC-26 and LoVo in vivo. NT may play an important role in growth regulation of certain colon cancers.",

keywords = "colon cancer, neurotensin",

author = "K. Yoshinaga and Evers, \{B. M.\} and M. Izukura and D. Parekh and T. Uchida and Townsend, \{C. M.\} and Thompson, \{J. C.\}",

note = "Funding Information: This work was supported by grants from the National Institute of Health (5R37 DK 15241, PO1 DK 35608) and the American Cancer Society (PDT 220). Funding Information: *Visiting Scientist from the Second Department of Surgery, Tokyo Medical and Dental University, Tokyo, Japan. TRecipient of an American Surgical Association Foundation Fellowship Award and a UTMB Small Grant Award. *Visiting Scientist from the First Department of Surgery, Osaka University Medical School, Osaka, Japan. §Visiting Scientist from the University of Witwatersrand, Johannesburg, South Africa; supported by scholarships from the Michael and Janie Miller Foundation and the Medical Research Council, South Africa.",

year = "1992",

month = apr,

doi = "10.1016/0960-7404(92)90025-G",

language = "English",

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T1 - Neurotensin stimulates growth of colon cancer

AU - Yoshinaga, K.

AU - Evers, B. M.

AU - Izukura, M.

AU - Parekh, D.

AU - Uchida, T.

AU - Townsend, C. M.

AU - Thompson, J. C.

N1 - Funding Information: This work was supported by grants from the National Institute of Health (5R37 DK 15241, PO1 DK 35608) and the American Cancer Society (PDT 220). Funding Information: *Visiting Scientist from the Second Department of Surgery, Tokyo Medical and Dental University, Tokyo, Japan. TRecipient of an American Surgical Association Foundation Fellowship Award and a UTMB Small Grant Award. *Visiting Scientist from the First Department of Surgery, Osaka University Medical School, Osaka, Japan. §Visiting Scientist from the University of Witwatersrand, Johannesburg, South Africa; supported by scholarships from the Michael and Janie Miller Foundation and the Medical Research Council, South Africa.

PY - 1992/4

Y1 - 1992/4

N2 - Neurotensin (NT), a peptide from the distal gut that is released by fat ingestion, stimulates the growth of normal small bowel and colonic mucosa. The purpose of this study was to determine whether chronic administration of NT would affect the growth of a mouse colon cancer (MC-26) and a human colon cancer (LoVo) in vivo. In experiment 1, male Balb/c mice were inoculated with MC-26 cells (5 × 104) and then randomized to four treatment groups receiving either saline (control) or NT (150, 300 or 600 μg kg-1) administered subcutaneously (s.c.) every 8 h for 21 days. In experiment 2, 60 mice with MC-26 tumours were randomized to receive saline (control) or NT (300 or 600 μg kg-1) for 28 days, and survival was then assessed. In experiment 3, 16 athymic nude mice with LoVo tumour xenografts were randomized to receive either saline (control) or NT (600 μg kg-1). We found that administration of NT (300 and 600 μg kg-1) significantly stimulated mean tumour area, weight and DNA, RNA and protein content of MC-26 tumours. In addition, the survival rate of mice bearing MC-26 tumours and treated with either dose of NT was significantly decreased compared with the control group given saline injections. Similarly, NT (600 μg kg-1) stimulated growth (tumour area, weight and nucleic acid contents) of the human colon cancer, LoVo. We conclude that NT acts as a trophic factor for the colon cancer cell lines MC-26 and LoVo in vivo. NT may play an important role in growth regulation of certain colon cancers.

AB - Neurotensin (NT), a peptide from the distal gut that is released by fat ingestion, stimulates the growth of normal small bowel and colonic mucosa. The purpose of this study was to determine whether chronic administration of NT would affect the growth of a mouse colon cancer (MC-26) and a human colon cancer (LoVo) in vivo. In experiment 1, male Balb/c mice were inoculated with MC-26 cells (5 × 104) and then randomized to four treatment groups receiving either saline (control) or NT (150, 300 or 600 μg kg-1) administered subcutaneously (s.c.) every 8 h for 21 days. In experiment 2, 60 mice with MC-26 tumours were randomized to receive saline (control) or NT (300 or 600 μg kg-1) for 28 days, and survival was then assessed. In experiment 3, 16 athymic nude mice with LoVo tumour xenografts were randomized to receive either saline (control) or NT (600 μg kg-1). We found that administration of NT (300 and 600 μg kg-1) significantly stimulated mean tumour area, weight and DNA, RNA and protein content of MC-26 tumours. In addition, the survival rate of mice bearing MC-26 tumours and treated with either dose of NT was significantly decreased compared with the control group given saline injections. Similarly, NT (600 μg kg-1) stimulated growth (tumour area, weight and nucleic acid contents) of the human colon cancer, LoVo. We conclude that NT acts as a trophic factor for the colon cancer cell lines MC-26 and LoVo in vivo. NT may play an important role in growth regulation of certain colon cancers.

KW - colon cancer

KW - neurotensin

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U2 - 10.1016/0960-7404(92)90025-G

DO - 10.1016/0960-7404(92)90025-G

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AN - SCOPUS:0026702097

SN - 0960-7404

VL - 1

SP - 127

EP - 134

JO - Surgical Oncology

JF - Surgical Oncology

IS - 2

ER -

Neurotensin stimulates growth of colon cancer

Resumen

Nota bibliográfica

Financiación

ODS de las Naciones Unidas

ASJC Scopus subject areas

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