research target：FLVCR1-AS1, miR-381-3p, CTNNB1, Breast cancer
Periodicals：Cancer Cell Int
IF：5.722
Cooperative Unit:Minhang Hospital of Fudan University
Time of publication：June, 2020
Summary
Background: Understanding the molecular mechanism of long non-coding RNAs (lncRNAs) in carcinogenesis is conducive for providing potential target for cancers. The role of FLVCR1-AS1 in breast cancer (BC) has not been probed yet.
Materials and methods: qRT-PCR and western blot assays were used to estimate relevant expressions of mRNAs and proteins. CCK8, MTT and EdU were implemented to assess cell proliferation ability. TUNEL was performed to investigate cell apoptosis, whereas transwell assay was performed to test cell migration and invasion capacities. TOP/FOP Flash assay was conducted to determine the activity of Wnt/β-catenin pathway. Luciferase reporter, RNA pull down and RIP assays were performed to verify interaction between genes.
Results: FLVCR1-AS1 was abnormally up-regulated in BC cells. Silencing FLVCR1-AS1 inhibited cell proliferation, migration, invasion, yet accelerating apoptosis. Inhibition of miR-381-3p reversed the tumor restraining impacts of FLVCR1-AS1 depletion on BC progression. Additionally, CTNNB1 was recognized to be targeted by miR-381-3p. FLVCR1-AS1 aggravated BC malignant progression via up-regulation CTNNB1 through sponging miR-381-3p.
Conclusion: FLVCR1-AS1 regulates BC malignant behavior via sequestering miR-381-3p and then freeing CTNNB1, implying a promising target for BC therapy.
Keywords: FLVCR1-AS1, miR-381-3p, CTNNB1, Breast cancer
Partial results of cooperation
BersinbioTM cooperative technology：FISH
Original link：10.1186/s12935-020-01247-2
