GROWTH-REGULATORY EFFECTS OF SENSORY NEUROPEPTIDES, EPIDERMAL GROWTH-FACTOR, INSULIN, AND SOMATOSTATIN ON THE NONTRANSFORMED INTESTINAL EPITHELIAL-CELL LINE IEC-6 AND THE COLON-CANCER CELL-LINE HT-29
GROWTH-REGULATORY EFFECTS OF SENSORY NEUROPEPTIDES, EPIDERMAL GROWTH-FACTOR, INSULIN, AND SOMATOSTATIN ON THE NONTRANSFORMED INTESTINAL EPITHELIAL-CELL LINE IEC-6 AND THE COLON-CANCER CELL-LINE HT-29
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DOI：
10.3109/00365529309103129
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发表时间：
1993-10-01
影响因子：
1.9
通讯作者：
JOHANSSON, C
中科院分区：
文献类型：
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作者：
BJORK, J;NILSSON, J;JOHANSSON, C
检测了未转化的大鼠小肠细胞系(IEC-6)和人结肠癌细胞系(HT29)对感觉神经肽的营养反应。检测P物质、神经激肽A(NKA)、降钙素基因相关肽(CGRP)、血管活性肠肽(VIP)和YY肽(PYY)。还使用了表皮生长因子(EGF)、胰岛素和生长抑素-14。将EGF或胰岛素与生长抑素-14结合，对IEC-6细胞进行相互作用研究。感觉神经肽对IEC-6细胞生长、DNA合成和HT29细胞生长均无影响。EGF和胰岛素对IEC-6细胞和HT29细胞的生长和DNA合成均有促进作用，且呈剂量依赖性。生长抑素-14单独或与EGF或胰岛素联合应用对IEC-6细胞生长和DNA合成均无影响。生长抑素-14只有在血清存在时才能抑制HT29细胞的生长，在10(-7)M时反应最大和显著。我们的观察表明，感觉神经肽对IEC-6细胞和HT29细胞都没有直接的生长调节作用。然而，生长抑素抑制血清诱导的HT29细胞的生长，但不直接干扰血清、EGF或胰岛素对IEC-6细胞的增殖作用。
A non-transformed small-intestinal cell line from the rat (IEC-6) and a human colon cancer cell line (HT 29) were examined for their trophic response to sensory neuropeptides. Substance P, neurokinin A (NKA), calcitonin gene-related peptide (CGRP), vasoactive intestinal peptide (VIP), and peptide YY (PYY) were tested. Epidermal growth factor (EGF), insulin, and somatostatin-14 were also used. Interaction studies were performed on IEC-6 cells by combining EGF or insulin with somatostatin-14. The sensory neuropeptides had no effect either on IEC-6 cell growth and DNA synthesis or on HT 29 cell growth. EGF and insulin stimulated cell growth and DNA synthesis in IEC-6 cells and cell growth in HT 29 cells in a dose-dependent fashion. Somatostatin-14 had no effect either alone or in combination with EGF or insulin on IEC-6 cell growth and DNA synthesis. HT29 cell growth was inhibited by somatostatin-14 only in the presence of serum with a maximal and significant response at 10(-7) M. Our observations suggest that the sensory neuropeptides do not exert a direct growth-regulatory effect either on IEC-6 cells or on HT 29 cells. Somatostatin, however, inhibits serum-induced HT 29 cell growth but does not interfere directly with the proliferative effect of serum, EGF, or insulin on IEC-6 cells in this model.