Expression of Insulin-Like Growth Factor Type 1 Receptor Is Linked to Inflammation in Adamantinomatous Craniopharyngioma

胰岛素样生长因子1受体 MAPK/ERK通路 内科学 内分泌学 胰岛素样生长因子 CD44细胞 生物 生长因子 癌症研究 医学 受体 激酶 细胞 细胞生物学 遗传学
作者
Lang Yang,Kai Li,Weizhao Li,Chaohu Wang,Liu Yi,Huarong Zhang,Jun Pan,Songtao Qi,Junxiang Peng
出处
期刊:Neuroendocrinology [S. Karger AG]
卷期号:112 (9): 917-926 被引量:1
标识
DOI:10.1159/000521458
摘要

<b><i>Introduction:</i></b> Insulin-like growth factor type 1 receptor (IGF1R) is overexpressed in various malignant tumors, which relates to their transformation and recurrence. Craniopharyngioma is a benign tumor with malignant results, often accompanied by a severe inflammatory reaction. However, the relationship between IGF1R expression and the inflammatory response of craniopharyngioma is unclear. <b><i>Methods:</i></b> We enrolled 85 patients with adamantinomatous craniopharyngioma (ACP) in a study to explore the relationship between IGF1R expression and clinical features of this disease. <b><i>Results:</i></b> Patients in the IGF1R high-expression group had a significantly higher incidence of hypopituitarism, higher recurrence rate, and lower progression-free survival. β-Catenin can further regulate expression of the stem cell marker, CD44, by regulating IGF1R. Using immunofluorescence, we found that tumor stem cell-like cells did not express phosphorylated (p)-ERK, although p-ERK activation was evident in the surrounding cells. Picropodophyllin, a specific inhibitor of IGF1R, increased the expression of p-ERK protein and decreased the transcription level of interleukin-6. <b><i>Conclusions:</i></b> High expression of IGF1R might promote inflammation of ACP, which might be an unfavorable factor for pituitary function and prognosis. The high expression of IGF1R in tumor stem cell-like cells might inhibit the expression of p-ERK and promote the generation of inflammatory factors. IGF1R plays a stemness maintenance role in ACP and regulates the production of inflammatory factors through a p-ERK pathway, which suggests that targeting IGF1R and p-ERK might provide a new direction for alleviating tumor inflammation.
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