Down-regulation of lncRNA BLACAT1 inhibits ovarian cancer progression by suppressing the Wnt/β-catenin signaling pathway via regulating miR-519d-3p

Ovarian cancer has the highest mortality in gynecologic malignancies. LncRNA BLACAT1 serves crucial functions in various cancers, but its role in ovarian cancer has not been investigated. In this article, our team explored the role and the potential regulatory mechanism of BLACAT1 in ovarian cancer....

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Bibliographic Details
Published in:Molecular and cellular biochemistry 2020-04, Vol.467 (1-2), p.95-105
Main Authors: Yang, Hua, Qi, Yue, Wang, Xin-lu, Gu, Jiao-jiao, Shi, Tie-mei
Format: Article
Language:English
Subjects:
Assaying
Biochemistry
Biomedical and Life Sciences
Cancer
Cardiology
Cell cycle
Cell migration
Cell proliferation
Flow cytometry
Immunohistochemistry
Life Sciences
Medical Biochemistry
miRNA
Oncology
Ovarian cancer
Polymerase chain reaction
Regulatory mechanisms (biology)
Ribonucleic acid
RNA
Signal transduction
Signaling
Wnt protein
Wound healing
β-Catenin
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Summary:Ovarian cancer has the highest mortality in gynecologic malignancies. LncRNA BLACAT1 serves crucial functions in various cancers, but its role in ovarian cancer has not been investigated. In this article, our team explored the role and the potential regulatory mechanism of BLACAT1 in ovarian cancer. Quantitative RT-PCR showed that BLACAT1 was aberrantly up-regulated in ovarian cancer tissues compared with normal tissues. In vitro, BLACAT1 knockdown induced cell cycle arrest and inhibited the proliferation, migration and invasion of ovarian cancer cells using flow cytometry, MTT and EdU assays, wound healing assay and transwell assay, respectively. Luciferase assay verified the binding relationship between microRNA-519d-3p and lncRNA BLACAT1, and BLACAT1 negatively regulated the expression of miR-519d-3p. We also found that miR-519d-3p overexpression could inhibit ovarian cancer cells proliferation, migration and invasion. Further, Western blot demonstrated that the expression of RPS15A and nuclear β-catenin expression was markedly reduced by BLACAT1 knockdown, and cytoplasmic β-catenin level was not obviously affected. In vivo, BLACAT1 knockdown inhibited the tumor growth, and immunohistochemistry showed that ki67 expression was decreased by BLACAT1 suppression. Inhibition of BLACAT1 was sufficient to down-regulate the expression of RPS15A and nuclear β-catenin but did not cause an obvious change in cytoplasmic β-catenin expression. Taken together, BLACAT1 knockdown inhibited the progression of ovarian cancer by suppressing the Wnt/β-catenin signaling pathway via regulating miR-519d-3p. Our work provided a proper understanding of the critical roles of BLACAT1 in ovarian cancer.
ISSN:0300-8177
1573-4919
DOI:10.1007/s11010-020-03704-y