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miR-635 targets KIFC1 to inhibit the progression of gastric cancer
  1. Feng-Yu Cao,
  2. Yong-Bin Zheng,
  3. Chao Yang,
  4. Su-Yang Huang,
  5. Xiao-Bo He,
  6. Shi-Lun Tong
  1. Gastrointestinal Surgery, Renmin Hospital of Wuhan University, Wuhan, China
  1. Correspondence to Dr Yong-Bin Zheng, Gastrointestinal Surgery, Renmin Hospital of Wuhan University, Wuhan, China; wqandzyb{at}


Accumulating studies have shown that the dysregulation of microRNAs is related to the carcinogenesis and development of gastric cancer (GC), and the role of miR-635 in GC remains largely unknown. miR-635 and Kinesin Family Member C1 (KIFC1) mRNA expression in GC tissues and paracancerous tissues and cells were detected by quantitative real-time PCR. KIFC1 protein expression in GC tissues and paracancerous normal tissues and cells was detected by immunohistochemistry and western blot. Cell proliferation was monitored by Cell Counting Kit-8 assay and 5-bromo-2′-deoxyuridine assay. Transwell assay was employed to detect the migration and invasion of GC cells. The dual-luciferase reporter gene assay was adopted to detect the targeting relationship between miR-635 and KIFC1. Compared with paracancerous tissues, miR-635 expression was remarkably decreased in GC tissues; conversely, KIFC1 expression was significantly increased. Compared with human normal gastric epithelial cell GSE-1, miR-635 expression was markedly decreased in GC cell lines. Meanwhile, KIFC1 expression was significantly increased, and the Kaplan-Meier Plotter database showed that its high expression was remarkably associated with poor prognosis. Additionally, miR-635 can negatively regulate KIFC1. miR-635 can target KIFC1 to inhibit proliferation, migration and invasion of GC cells. Collectively, miR-635 is lowly expressed in GC, and it inhibits proliferation, migration and invasion of GC cells via regulating KIFC1.

  • gastric mucosa

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  • Contributors F-YC and Y-BZ conceived and designed the experiments, F-YC, CY, S-YH and X-BH performed the experiments, S-YH carried out the statistical analysis, F-YC and S-LT wrote the paper. All authors read and approved the final manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Ethics approval Our study was approved by the ethics review board of Renmin Hospital of Wuhan University (approval number: 2017F014).

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data availability statement Data are available upon reasonable request. The data used to support the findings of this study are available from the corresponding author upon request.