Highlights
- •The expression of circ_0108942 was upregulated in BC.
- •Circ_0108942 knockdown inhibited cell proliferation, migration, invasion, and angiopoiesis, and promoted apoptosis in BC cells.
- •Circ_0108942 promoted the progression of BC by sponging miR-1178-3p.
- •MiR-1178-3p inhibited BC progression by targeting TMED3.
Abstract
Background
Breast cancer (BC) has posed a fatal threat to women's lives and the search for new
methods of diagnosis and treatment is an important way to break the bottleneck of
high mortality in BC. Circular RNAs (circRNAs) have been confirmed to be aberrantly
expressed in several types of cancers, and this study is intended to elucidate the
role and mechanism of circ_0108942 in BC.
Materials and Methods
The levels of circ_0108942, microRNA-1178-3p (miR-1178-3p), and transmembrane p24
trafficking protein 3 (TMED3) were measured using real-time quantitative polymerase
chain reaction (RT-qPCR) or western blot. Meanwhile, the cell proliferation, migration,
invasion, angiopoiesis, and apoptosis were analyzed using 5-ethynyl-2′-deoxyuridine
(EdU), transwell, tubule formation, and flow cytometry assays. Protein levels were
determined by western blot. In addition, we used dual-luciferase reporter and RNA
pull-down assays to identify the interplay between miR-1178-3p and circ_0108942 or
TMED3. Lastly, the impact of circ_0108942 on the growth of BC tumors in vivo was analyzed by xenograft models.
Results
Circ_0108942 and TMED3 were notably upregulated in BC, and the miR-1178-3p was downregulated.
Functionally, silencing circ_0108942 suppressed cell proliferation, migration, invasion
and promoted apoptosis in BC cells. In mechanism, circ_0108942 regulated TMED3 expression
by sponging miR-1178-3p. Meanwhile, circ_0108942 knockdown also greatly constrained
tumor growth in vivo.
Conclusion
Circ_0108942 boosted BC progression by regulating miR-1178-3p and thus upregulating
TMED3.
Keywords
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Article info
Publication history
Published online: December 22, 2022
Accepted:
December 19,
2022
Received in revised form:
September 21,
2022
Received:
April 23,
2022
Publication stage
In Press Journal Pre-ProofIdentification
Copyright
© 2022 Elsevier Inc. All rights reserved.