Long noncoding RNA XIST expedites metastasis and modulates epithelial–mesenchymal transition in colorectal cancer

نویسندگان

  • Dong-liang Chen
  • Le-zong Chen
  • Yun-xin Lu
  • Dong-sheng Zhang
  • Zhao-lei Zeng
  • Zhi-zhong Pan
  • Peng Huang
  • Feng-hua Wang
  • Yu-hong Li
  • Huai-qiang Ju
  • Rui-hua Xu
چکیده

Tumor progression and metastasis is the main cause of death in colorectal cancer (CRC). Long noncoding RNAs (lncRNAs) are critical regulators in various diseases including human cancer. In this study, we found that lncRNA XIST was overexpressed in CRC cell lines and tissues. High expression of lncRNA XIST was associated with adverse overall survival in CRC patients. Knockdown of lncRNA XIST remarkably inhibited CRC cell proliferation, invasion, epithelial-mesenchymal transition (EMT) and CRC stem cell formation in vitro as well as tumor growth and metastasis in vivo. Further study indicated that knockdown of lncRNA XIST markedly increased the expression of microRNA-200b-3p (miR-200b-3p) that has been found to be downregulated in CRC tissues and cell lines, and luciferase activity assay indicated that lncRNA XIST could bind directly with miR-200b-3p. Moreover, knockdown of lncRNA XIST significantly reduced the expression of ZEB1, which was the direct target of miR-200b-3p, and the tumor suppressive effects caused by knockdown of lncRNA XIST could be rescued by re-expression of ZEB1 in CRC cells. Overall, our study demonstrated how lncRNA XIST regulates CRC progression and metastasis by competing for miR-200b-3p to modulate the expression of ZEB1. lncRNA XIST may be used as a biomarker to predict prognosis in CRC patients.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Mesenchymal Stem Cells Trigger Epithelial to Mesenchymal Transition in the HT-29 Colorectal Cancer Cell Line

Background and Objective: Mesenchymal stem cells (MSCs) promote metastasis in colorectal cancer; however, the mechanism underlying this process is not fully understood. Epithelial to mesenchymal transition (EMT) is a key step in tumor acquisition of metastatic phenotype. We aimed to investigate the effect of MSCs on the expression of EMT markers, as well as cancer stem cell markers in HT-29 col...

متن کامل

Long noncoding RNA SPRY4-IT1 promotes malignant development of colorectal cancer by targeting epithelial–mesenchymal transition

The clinical significance and biological functions of long noncoding RNA SPRY4 intronic transcript 1 (SPRY4-IT1) in colorectal cancer (CRC) remain largely unclear. Herein, we are the first to report that the SPRY4-IT1 was significantly upregulated in CRC tissues, serum, and cells. Higher SPRY4-IT1 expression was markedly associated with advanced Tumor Node Metastasis (TNM) stage in a cohort of ...

متن کامل

Epithelial to mesenchymal transition concept in Cancer: Review article

Owing to this fact that most of the mortalities in cancers are as a result of metastasis, study on the involved pathways in metastasis including Epithelial to mesenchymal transition (EMT) would be so critical and important. Up to date, several extensive studies have been carried out to determine the correlation between EMT and cancer and their results have shown that the EMT plays pivotal role ...

متن کامل

Analysis of epithelial mesenchymal transition markers in breast cancer cells in response to stromal cell-derived factor 1

Introduction: Metastasis is the main cause of cancer death; however, the underlying mechanisms of metastasis are largely unknown. The chemokine of stromal cell-derived factor 1 (SDF1) and the process of epithelial mesenchymal transition (EMT), both have been declared as important factors to promote cancer metastasis; however, Conspicuously, the relation between them has not been recognized well...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 8  شماره 

صفحات  -

تاریخ انتشار 2017