Research Papers:

MiR-19b suppresses PTPRG to promote breast tumorigenesis

Minghui Liu, Rong Yang, Uzair Urrehman, Chao Ye, Xin Yan, Shufang Cui, Yeting Hong, Yuanyuan Gu, Yanqing Liu, Chihao Zhao, Liang Yan, Chen-Yu Zhang, Hongwei Liang and Xi Chen _

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Oncotarget. 2016; 7:64100-64108. https://doi.org/10.18632/oncotarget.11799

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Minghui Liu1,*, Rong Yang1,2,*, Uzair Urrehman1,*, Chao Ye1, Xin Yan3, Shufang Cui1, Yeting Hong1, Yuanyuan Gu1, Yanqing Liu1, Chihao Zhao1, Liang Yan4, Chen-Yu Zhang1, Hongwei Liang1, Xi Chen1

1State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Center for MicroRNA Biology and Biotechnology, NJU Advanced Institute for Life Sciences (NAILS), School of Life Sciences, Nanjing University, Nanjing, Jiangsu 210046, China

2Department of Urology, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, Jiangsu 210008, China

3Department of Respiratory Medicine, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, Jiangsu 210008, China

4Provincial Key Laboratory of Biological Macro-molecules Research, Wannan Medical College, Wuhu, Anhui 241002, China

*These authors contributed equally to this work

Correspondence to:

Xi Chen, email: [email protected]

Hongwei Liang, email: [email protected]

Chen-Yu Zhang, email: [email protected]

Keywords: miR-19b, PTPRG, proliferation, apoptosis, migration

Received: January 05, 2016     Accepted: August 22, 2016     Published: September 01, 2016


Protein tyrosine phosphatase receptor type G (PTPRG) is an important tumor suppressor gene in multiple human cancers. In this study, we found that PTPRG protein levels were downregulated in breast cancer tissues while the mRNA levels varied irregularly, implying a post-transcriptional mechanism was involved. Because microRNAs are powerful post-transcriptional regulators of gene expression, we used bioinformatics analysis to search for microRNAs that potentially targets PTPRG in the setting of breast cancer. We identified two specific binding sites for miR-19b in the 3′-untranslated region of PTPRG. We further identified an inverse correlation between miR-19b and PTPRG protein levels, but not mRNA levels, in human breast cancer tissues. By overexpressing or knocking down miR-19b in MCF-7 cells and MDA-231 cells, we experimentally confirmed that miR-19b directly suppresses PTPRG expression. Furthermore, we determined that the inhibition of PTPRG by miR-19b leads to increased proliferation, stimulated cell migration and reduced apoptosis. Taken together, our findings provide the first evidence that miR-19b inhibits PTPRG expression to promote tumorigenesis in human breast cancer.

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