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LncRNA PART1 Promotes Breast Cancer Cell Progression by Directly Targeting MiR-4516

Overview
Publisher Dove Medical Press
Specialty Oncology
Date 2020 Sep 14
PMID 32922076
Citations 14
Authors
Affiliations
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Abstract

Introduction: Breast cancer is a serious threat to human health. It is meaningful to study the pathogenesis of breast cancer. lncRNAs have been found to play vital roles in numerous biological processes including development, immunology and cancer.

Methods: qRT-PCR was performed to examine the expressions of PART1 and miR-4516. CCK-8 assay, colony formation assay and transwell assay were used to examine the progression of breast cancer cells.

Results: In this study, we showed that lncRNA PART1 was highly expressed in breast cancer cells. Knockdown of PART1 induced decreased proliferation, invasion and migration of breast cancer cells. Moreover, we found that PART1 can bind to miR-4516 directly. We also found that inhibition of miR-4516 could rescue the decreased proliferation, migration and invasion of breast cancer cells induced by knockdown of PART1.

Discussion: lncRNA PART1 and miR-4516 were proven to be involved in the progression of many cancers. However, the roles of lncRNA PART1 and miR-4516 in the regulation of breast cancer remain unknown. Here, we demonstrated that PART1 can bind to miR-4516 to decrease the expression of miR-4516 and promote the development of breast cancer.

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References
1.
Kong Q, Qiu M . Long noncoding RNA SNHG15 promotes human breast cancer proliferation, migration and invasion by sponging miR-211-3p. Biochem Biophys Res Commun. 2017; 495(2):1594-1600. DOI: 10.1016/j.bbrc.2017.12.013. View

2.
Chowdhari S, Saini N . hsa-miR-4516 mediated downregulation of STAT3/CDK6/UBE2N plays a role in PUVA induced apoptosis in keratinocytes. J Cell Physiol. 2014; 229(11):1630-8. DOI: 10.1002/jcp.24608. View

3.
Li M, Zhang W, Zhang S, Wang C, Lin Y . PART1 expression is associated with poor prognosis and tumor recurrence in stage I-III non-small cell lung cancer. J Cancer. 2017; 8(10):1795-1800. PMC: 5556642. DOI: 10.7150/jca.18848. View

4.
Kang M, Ren M, Li Y, Fu Y, Deng M, Li C . Exosome-mediated transfer of lncRNA PART1 induces gefitinib resistance in esophageal squamous cell carcinoma via functioning as a competing endogenous RNA. J Exp Clin Cancer Res. 2018; 37(1):171. PMC: 6063009. DOI: 10.1186/s13046-018-0845-9. View

5.
Wang J, Liu H, Li M . Downregulation of miR-505 promotes cell proliferation, migration and invasion, and predicts poor prognosis in breast cancer. Oncol Lett. 2019; 18(1):247-254. PMC: 6540292. DOI: 10.3892/ol.2019.10334. View