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Estrogen facilitates gastric cancer cell proliferation and invasion through promoting the secretion of interleukin-6 by cancer-associated fibroblasts

雌激素 细胞生长 癌症研究 癌相关成纤维细胞 生物 MMP2型 免疫印迹 癌细胞 细胞 癌症 细胞迁移 分子生物学 内分泌学 转移 生物化学 遗传学 基因
作者
Shouxin Zhang,Xiliang Cong,Zhiguo Li,Yingwei Xue
出处
期刊:International Immunopharmacology [Elsevier]
卷期号:78: 105937-105937 被引量:27
标识
DOI:10.1016/j.intimp.2019.105937
摘要

As a common disease, gastric cancer (GC) has influenced over 1 million people worldwide. Despite of prevention and optimal treatments, GC still has a high mortality. The role of cancer-associated fibroblasts (CAFs) in tumor progression has recently attracted attention, yet few studies have focused on GC. Estrogen has been reported to relate to the poor prognosis of GC. Therefore, we investigated whether estrogen can stimulate CAFs to produce tumor promoting factors in this study. Gastric CAFs were isolated from GC tissues and treated with estrogen. ELISA results suggested that CAFs produced interleukin-6 (IL-6) after estrogen treatment in a dose-dependent manner. The cell culture supernatant for estrogen-treated CAFs was collected and used as conditioned medium (CM) for GC cells. After cultured in CM, increased cell proliferation and alteration of cell cycle were detected by CCK-8 assay, BrdU assay, and flow cytometry. Western blot and gelatin zymography were used to determine cancer invasion-associated proteins. Results indicated that the expression of matrix metalloproteinase 2 (MMP2) and MMP9 were enhanced by Estrogen-CAFs-CM. Additional transwell assay showed that cell invasion and migration were promoted after cultured in CM. Lastly, western blot and immunofluorescence results demonstrated that the level of phosphorylated signal transducer and activator of transcription 3 (STAT3) in GC cells increased after cultured in CM. The effect was neutralized by IL-6 neutralizing antibody and STAT3 siRNA. Conclusively speaking, estrogen can activate CAFs to produce IL-6, ending up with promotion of GC cell proliferation and invasion. This result may suggest a new therapeutic target for GC.
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