Downregulation of lncRNA MEG3 and miR-770-5p inhibit cell migration and proliferation in Hirschsprung’s disease

نویسندگان

  • Hongxing Li
  • Bo Li
  • Dongmei Zhu
  • Hua Xie
  • Chunxia Du
  • Yankai Xia
  • Weibing Tang
چکیده

The long noncoding RNA (lncRNA) MEG3 is involved in various biological processes including cell migration and cell proliferation. In present study, it was found that MEG3 and the intronic miR-770-5p were decreased in samples from HSCR patients. Besides, knockdown of MEG3 and miR-770-5p suppressed cell migration and proliferation, while cell cycle and apoptosis were not affected in human 293T and SH-SY5Y cells. SRGAP1 mRNA and protein upregulation was inversely correlated with miR-770-5p expression in tissue samples and cell lines, which was confirmed to be a target gene of miR-770-5p by dual-luciferase reporter assay. Moreover, silencing of SRGAP1 rescued the inhibition of cell migration and proliferation induced by MEG3 siRNA and miR-770-5p inhibition. The present study elucidates a novel mechanism of the development of HSCR and shows that the MEG3/miR-770-5p/SRGAP1 pathway plays a vital role in the pathogenesis of HSCR.

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

Downregulation of TMEM40 by miR-138-5p suppresses cell proliferation and mobility in clear cell renal cell carcinoma

Background: Clear cell renal cell carcinoma (ccRCC) represents approximately 70% of RCC,as the most frequent histological subtype of RCC. MiR-138-5p, a tumor-related microRNA (miRNA), has been reported to be implicated in the diverse types of human malignancies, but its role in ccRCCremains unclear. Objective: The study was designed to investigate the function...

متن کامل

LncRNA MEG3 enhances cisplatin sensitivity in non-small cell lung cancer by regulating miR-21-5p/SOX7 axis

Background Long noncoding RNAs (lncRNAs) have been revealed to play essential role in drug resistance of multiple cancers. LncRNA MEG3 was previously reported to be associated with cisplatin (DDP) resistance in non-small cell lung cancer (NSCLC) cells. However, the molecular mechanism of MEG3 affecting DDP resistance in NSCLC remains to be further illustrated. In this study, we attempted to dis...

متن کامل

LncRNA Miat Promotes Proliferation of Cervical Cancer Cells and Acts as an Anti-apoptotic Factor

There are a sub-population of cells in tumor tissues known as cancer stem cells (CSCs) which have similar features with stem cells, including self-renewal and differentiation capacity. Recently, it was established that not only stem cells factors such as Oct4, but also ES-associated lncRNAs are contributing to various regulatory aspects of CSCs. Myocardial infarction associated transcript (MIAT...

متن کامل

Long noncoding RNA MEG3 suppressed endothelial cell proliferation and migration through regulating miR-21.

Long non-coding RNAs (lncRNAs) act critical roles in many biological processes, including cell proliferation, apoptosis, development, invasion and migration. LncRNA maternally expressed gene 3 (MEG3) is found to be downregulated in several tumors; however, its role in the atherosclerosis is still unknown. In the present study, we demonstrated that MEG3 expression level was downregulated in the ...

متن کامل

Radiation-inducible miR-770-5p sensitizes tumors to radiation through direct targeting of PDZ-binding kinase

Radiotherapy represents the most effective non-surgical modality in cancer treatment. MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression, and are involved in many biological processes and diseases. To identify miRNAs that influence the radiation response, we performed miRNA array analysis using MCF7 cells at 2, 8, and 24 h post irradiation. We demonstrated that miR-770-5...

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