4.6 Article

miR-875-5p exerts tumor-promoting function via down-regulation of CAPZA1 in esophageal squamous cell carcinoma

Journal

PEERJ
Volume 9, Issue -, Pages -

Publisher

PEERJ INC
DOI: 10.7717/peerj.10020

Keywords

ESCC; miR-875-5p; SNP; CAPZA1; Down-regulate

Funding

  1. National Natural Science Foundation of China [81830086, 81988101]
  2. Beijing Nova Program [xx2018040]
  3. CAMS Initiative for Innovative Medicine [2017-I2M-3-004]
  4. Research and Development Funding of Peking University People's Hospital [RDY2018-08]

Ask authors/readers for more resources

ESCC is one of the leading causes of cancer deaths worldwide, and miR-875-5p can promote the proliferation, invasion, and migration of ESCC cells by down-regulating CAPZA1 expression.
Esophageal squamous cell carcinoma (ESCC) is one of the leading causes of cancer deaths worldwide. Currently, efficient genetic markers for diagnosis and treatment of ESCC are lacking. MicroRNAs (miRNAs) are global genetic regulators that control cancer gene expression by binding to the 3'untranslated regions (3'UTRs) of targeting mRNAs. In addition, miRNAs function as oncogenes or tumor suppressors in the progression of tumors. In the current study, we found that hsa-miR-875-5p (miR-875-5p) exhibited amplification in ESCC according to the TCGA database. Then, xCELLigence Real-Time Cell Analyzer (RTCA)-MP system and colony formation assays were employed to detect cell proliferationand colony formationability. The results showed that miR-875-5p promoted the proliferation ESCC cells. Subsequently, transwell results indicated that miR-875-5p promoted the invasion and migration of ESCC cells. Furthermore, we showed that miR-875-5p was able to bind to CAPZA13'UTR, which contains the single nucleotide polymorphism (SNP), rs373245753, as reported in our previous study involving WGS and WES on ESCC. Subsequently, mRNA affinity pull-down assays verifiedthat the SNP disrupts miR-875-5p binding to CAPZA1. The current study is the first demonstration that miR-875-5p may function as an oncogene via down-regulation of CAPZA1 expression in ESCC.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.6
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available