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. 2005 Jun 7;11(21):3217-21.
doi: 10.3748/wjg.v11.i21.3217.

Expression of some tumor associated factors in human carcinogenesis and development of gastric carcinoma

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Expression of some tumor associated factors in human carcinogenesis and development of gastric carcinoma

Ming-Dong Zhao et al. World J Gastroenterol. .

Abstract

Aim: To study the effect of IGF-1/IGF-1R and gastrin/CCK-BR on carcinogenesis and development of human gastric carcinoma and to explore its mechanism and provide a credible theoretical foundation for early diagnosis and molecular therapy of gastric carcinoma.

Methods: mRNA expression levels of IGF-1/IGF-1R and gastrin/CCK-BR were assessed by RT-PCR method in gastric cancer tissues, adjacent mucosa, and tumor-free tissues from 56 patients with gastric carcinoma and normal gastric mucosae from 56 healthy controls. Tissue specimens were obtained by biopsy and confirmed by histological evaluation.

Results: The mRNA levels of IGF-1/IGF-1R were increased in gastric cancer tissues compared with normal tissues from healthy controls and successively increased in tumor-free tissues, adjacent mucosa, and gastric cancer tissues. The mRNA levels of gastrin/CCK-BR were increased in gastric cancer tissues compared with normal tissues from healthy controls. There was a significant difference between gastric cancer tissues and adjacent mucosa and tumor-free tissues, but the mRNA levels of gastrin were not significantly increased in adjacent mucosa and gastric cancer tissues compared with tumor-free tissues. The mRNA levels of CCK-BR were increased in gastric cancer tissues and adjacent mucosa compared with tumor-free tissues, but not significantly increased in adjacent mucosa and gastric cancer tissues compared with gastric cancer tissues.

Conclusion: Overexpression of IGF-1/IGF-1R and gastrin/CCK-BR promotes the disorderly proliferation of gastric mucosa epithelia and it is of great significance in the carcinogenesis and development of gastric carcinoma.

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Figures

Figure 1
Figure 1
mRNA expression of IGF-1/IGF-1R and gastrin/CCK-BR in gastric cancer tissues and normal mucosa from control bP<0.01 vs control.
Figure 2
Figure 2
RT-PCR amplified products of IGF-1/β-actin. A: IGF-1R/β-actin; B: gastrin/β-actin; C: and CCK-BR/β-actin; D: detected by electrophoresis on an 1.8% agarose gel. Lane 1: gastric cancer tissues; lane 2: adjacent mucosa; lane 3: tumor-free tissues; lane 4: healthy controls; M: standard molecular weight of DNA.

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References

    1. Konturek PC, Konturek SJ, Sulekova Z, Meixner H, Bielanski W, Starzynska T, Karczewska E, Marlicz K, Stachura J, Hahn EG. Expression of hepatocyte growth factor, transforming growth factor alpha, apoptosis related proteins Bax and Bcl-2, and gastrin in human gastric cancer. Aliment Pharmacol Ther. 2001;15:989–999. - PubMed
    1. Han SU, Lee JH, Kim WH, Cho YK, Kim MW. Significant correlation between serum level of hepatocyte growth factor and progression of gastric carcinoma. World J Surg. 1999;23:1176–1180. - PubMed
    1. Torrisi R, Mezzetti M, Johansson H, Barreca A, Pigatto F, Robertson C, Decensi A. Time course of fenretinide-induced modulation of circulating insulin-like growth factor (IGF)-i, IGF-II and IGFBP-3 in a bladder cancer chemoprevention trial. Int J Cancer. 2000;87:601–605. - PubMed
    1. Blakesley VA, Stannard BS, Kalebic T, Helman LJ, LeRoith D. Role of the IGF-I receptor in mutagenesis and tumor promotion. J Endocrinol. 1997;152:339–344. - PubMed
    1. Baserga R. The IGF-I receptor in cancer research. Exp Cell Res. 1999;253:1–6. - PubMed

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