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RETRACTED: MiR‐137 functions as a tumor suppressor in pancreatic cancer by targeting MRGBP
Author(s) -
Ding Feng,
Zhang Shuang,
Gao Shaoyang,
Shang Jian,
Li Yanxia,
Cui Ning,
Zhao Qiu
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.26676
Subject(s) - pancreatic cancer , panca , gene silencing , microrna , cancer research , transfection , biology , carcinogenesis , apoptosis , downregulation and upregulation , epigenetics , cancer , cell growth , cell culture , medicine , pathology , gene , genetics , vasculitis , disease , anti neutrophil cytoplasmic antibody
miRNAs are small noncoding RNAs that act as critical epigenetic regulators in tumor carcinogenesis. In this study, our data showed that miR‐137 was significantly downregulated in 58 pairs of human pancreatic cancer (PanCa) tissues and PanCa cell lines. Furthermore, the deregulated miR‐137 was correlated with increased tumor size, higher TNM stage, and worse prognosis in pancreatic cancer. Functional studies demonstrated that overexpression of miR‐137 dramatically suppressed cell proliferation and induced cell apoptosis in vitro. Meanwhile, upregulated miR‐137 remarkably inhibited migration and invasion of pancreatic cancer cells. Further studies indicated that MRGBP was identified as the direct downstream target gene of miR‐137. In addition, MRGBP expression is significantly downregulated in miR‐137‐transfected cells. Our previous study revealed that silencing of MRGBP suppressed the growth of PanCa cells in vitro and in vivo and also promoted apoptosis, and inhibited migration and invasion of PanCa cells, which are consistent with the effects of miR‐137 overexpression. Taken together, our findings suggest that miR‐137 may function as a novel tumor promoter through directly targeting MRGBP in PanCa.