| Literature DB >> 30958882 |
Jing Wu1,2,3, Xuan Feng1,2,3, Yan Du1,2, Baoxin Luan1,2,3, Huandi Yu1,2,3, Yinhua Yu1,2,3, Lanxiang Wu4, Hongbo Zhao1,2,3.
Abstract
Choriocarcinoma is a rare and malignant trophoblastic tumor. However, the molecular mechanisms by which choriocarcinoma is regulated remain unknown. In the present study, we first elucidated that LIN28B was highly expressed in human choriocarcinoma tissues and choriocarcinoma cell lines. Our data further demonstrated that knockdown of LIN28B by small interfering RNA caused an increase in Let-7a expression in JAR cells. In addition, silencing of LIN28B inhibited IGF2BP1 expression and suppressed cell proliferation capacity, both of which can be markedly restored by Let-7a inhibitor. In contrast, LIN28B over-expression-improved cell proliferation was inhibited by Let-7a mimic. Knockdown of β-catenin resulted in reduced expression of LIN28B and increased expression of Let-7a. Knockdown of β-catenin also caused a decrease in cell proliferation, which can be recovered by re-expression of LIN28B or by Let-7a inhibitor. Collectively, our data indicate that β-catenin/LIN28B/Let-7a pathway may be crucial for the regulation of cell proliferation in human choriocarcinoma cells.Entities:
Keywords: LIN28B; Let-7a; cell proliferation; choriocarcinoma; β-catenin
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Year: 2019 PMID: 30958882 DOI: 10.1093/abbs/gmz027
Source DB: PubMed Journal: Acta Biochim Biophys Sin (Shanghai) ISSN: 1672-9145 Impact factor: 3.848