Upregulated exosomic miR‑23b‑3p plays regulatory roles in the progression of pancreatic cancer.

外泌体 miR'23b'3p 上调在胰腺癌的进展中发挥调控作用

阅读:8
作者:Chen Dayang, Wu Xiongbo, Xia Min, Wu Fang, Ding Junli, Jiao Yang, Zhan Qiang, An Fangmei
Pancreatic cancer (PC) is one of the most lethal malignances. Identification of biomarkers for early diagnosis of PC is a key imperative. MicroRNAs (miRNAs) have been shown to be valuable biomarkers in the context of several cancers. Exosomes refer to vesicles released by the tumor cells at the early stage of disease. Thus, detection of miRNA in exosomes can be used as a potential biomarker for PC. In this study, we profiled serum levels of miRNAs in patients with chronic pancreatitis (CP) and PC; the role of miR‑23b‑3p in PC progression was assessed in vitro. Additionally, we assessed, the expression of miR‑23b‑3p in exosomes isolated from serum samples and assessed the correlation between the expression of miR‑23b‑3p and carbohydrate antigen 19-9 (CA19-9). Three serum samples each were randomly selected from healthy controls (n=20), and patients with CP (n=18) and PC (n=16) for miRNA microarray profiling. The dysregulated miRNAs were confirmed using qRT‑PCR. Four dysregulated miRNAs common to patients with CP and PC were identified on miRNA microarray analysis and confirmed by qRT‑PCR. miR‑23b‑3p level was consistently higher in serum samples from PC patients as compared to those from healthy controls and CP patients (p<0.05). Overexpression of miR‑23b‑3p promoted proliferation, migration, and invasion capability of PC cells in vitro (p<0.05). Furthermore, miR‑23b‑3p was upregulated in exosomes of PC serum samples and the supernatant of pancreatic cancer cells (PANC‑1), and the expression levels of miR‑23b‑3p were associated with those of serum CA19-9 levels. This study provides insights into the potential role of miR‑23b‑3p as a novel biomarker and target for treatment of PC.

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。