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

• DOI: 10.2147/ott.s93056
• Publication Date: 2015-10-28T23:09:08Z
• Authors: Shijie Ma; Xiaoling Luo; Shiyan Yang; Chuanwen Zhou; Feng Pan; Qianjun Li
• Keywords: 0301 basic medicine; 03 medical and health sciences; OncoTargets and Therapy; Original Research; 3. Good health

Interaction between microRNA (miR-328) and PTPRJ (protein tyrosine phosphatase, receptor type, J) has been reported to be responsible for miR-328-dependent increase in epithelial cancer cell proliferation. However, the role of miR-328 hepatocellular carcinoma (HCC) remains unclear. The aim this study was investigate clinical significance and/or expression human HCC determine their precise biological functions malignancy.Expression levels messenger RNA (mRNA) 100 pairs adjacent noncancerous tissues were detected using quantitative real-time reverse transcription polymerase chain reaction. associations various clinicopathological features patients further statistically assessed. Then, migration invasion two lines determined by transwell assays.miR-328 mRNA markedly upregulated down-regulated tissues, respectively, compared tissues. Notably, upregulation significantly correlated with downregulation (r=-0.362, P=0.01). In addition, miR-328-high PTPRJ-low found closely high Edmondson-Steiner grading (all P<0.05) advanced tumor-node-metastasis stage P<0.05). Moreover, restoration dramatically promoted repressing expression. Interestingly, loss could attenuate inhibitory effects knockdown on cells.These findings demonstrated that dysregulation may associated tumor progression patients. Functionally, serve as a crucial oncogene implicated motility cells at least part suppression PTPRJ.