MicroRNA-328 enhances cellular motility through posttranscriptional regulation of PTPRJ in human hepatocellular

Xiaoling Luo1, Shiyan Yang2, Chuanwen Zhou1

  • 1Department of Gastroenterology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu, People's Republic of China.

Oncotargets and Therapy
|November 26, 2015
PubMed
Abstract

Insights

MicroRNA-328 (miR-328) is upregulated and protein tyrosine phosphatase, receptor type, J (PTPRJ) is downregulated in hepatocellular carcinoma (HCC). This dysregulation promotes HCC cell migration and invasion, indicating miR-328

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • MicroRNA (miR-328) and protein tyrosine phosphatase, receptor type, J (PTPRJ) interactions are linked to epithelial cancer cell proliferation.
  • The specific roles of miR-328 and PTPRJ in hepatocellular carcinoma (HCC) are not well understood.

Purpose of the Study:

  • To investigate the clinical significance of miR-328 and PTPRJ expression in human HCC.
  • To determine the precise biological functions of miR-328 and PTPRJ in HCC progression.

Main Methods:

  • Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) was used to measure miR-328 and PTPRJ mRNA levels in 100 HCC and adjacent noncancerous tissue pairs.
  • Statistical analysis assessed correlations between miR-328/PTPRJ expression and HCC clinicopathological features.
  • Transwell assays evaluated the functional roles of miR-328 and PTPRJ in HCC cell migration and invasion.

Main Results:

  • miR-328 mRNA was upregulated, while PTPRJ mRNA was downregulated in HCC tissues compared to noncancerous tissues.
  • miR-328 upregulation significantly correlated with PTPRJ downregulation in HCC (r=-0.362, P=0.01).
  • High miR-328 and/or low PTPRJ expression correlated with advanced Edmondson-Steiner grading and tumor-node-metastasis (TNM) stage.
  • Restoring miR-328 promoted HCC cell migration and invasion by repressing PTPRJ; loss of PTPRJ attenuated miR-328 knockdown effects.

Conclusions:

  • Dysregulation of miR-328 and PTPRJ is associated with HCC tumor progression.
  • miR-328 functions as an oncogene in HCC, promoting cell motility partly through PTPRJ suppression.

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