MicroRNA 214 inhibits adipocyte enhancer-binding protein 1 activity and increases the sensitivity of chemotherapy in colorectal cancer

MicroRNA 214 抑制脂肪细胞增强子结合蛋白 1 活性并增加结直肠癌化疗的敏感性

阅读:6
作者:Shouchao Li, Chengren Li, Zhiming Fang

Abstract

The present study aimed to analyze adipocyte enhancer-binding protein 1 (AEBP1) expression in colorectal cancer (CRC), with a focus on its possible molecular mechanisms, in order to provide novel insight into the clinical treatment of CRC. Immunohistochemistry (IHC) was used to detect AEBP1 expression in 62 CRC tissues. Kaplan-Meier survival curves were used to analyze AEBP1 expression and the postoperative disease-free survival (DFS) and overall survival (OS) rates of CRC patients. HT-29 cells were treated with oxaliplatin to detect cell proliferation and apoptosis following a Cell Counting kit-8. Through bioinformatics prediction, microRNA 214 (miR214) was identified as an upstream microRNA of AEBP1 that regulates its expression. IHC revealed that the expression of AEBP1 in CRC tissues was significantly higher than that in adjacent healthy tissues, and that it is associated with Tumor-Node-Metastasis stage, recurrence and metastasis. The DFS and OS rates of patients with a low AEBP1 expression were significantly higher than those in patients with a high expression (P<0.05). Following depletion of AEBP1 and treatment with oxaliplatin, the HT-29 cell proliferation was lower than that of the blank control and the negative control groups. However, the cell apoptosis rate was higher than that of the control group at 72 h (P<0.05). Bioinformatics prediction revealed that miR-214 is negatively associated with AEBP1 expression, and co-transfection and luciferase report gene tests revealed that AEBP1 is a target gene of miR-214. Therefore, AEBP1 may become a novel treatment for CRC patients with chemoresistance and may act through the upstream miR-214 to participate in the progression of a tumor.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。