Highlights
- •Hsa_circ_0008673 was markedly elevated in BC tissues and cells.
- •Down-regulation of hsa_circ_0008673 increased cell apoptosis.
- •Hsa_circ_0008673 regulated the expression of GINS4 by sponging miR-578.
- •GINS4 was responsible for BC progression regulated by hsa_circ_0008673.
Abstract
Background
Circular RNAs (circRNAs) play a crucial role in breast cancer (BC) development. This
study aimed to explore the new potential mechanism of hsa_circ_0008673 in BC.
Materials and Methods
Hsa_circ_0008673, microRNA-578 (miR-578) and recombinant human GINS complex subunit
4 (GINS4) abundances were measured via quantitative real-time PCR or western blot.
Cell proliferation, metastasis, angiogenesis and apoptosis were assessed via EdU assay,
transwell assay, tube formation assay, and flow cytometry. The interactions among
hsa_circ_0008673, miR-578 and GINS4 were tested via dual-luciferase reporter analysis
and RNA pull-down assay. Animal studies were performed to assess the effect of hsa_circ_0008673
on BC tumor growth.
Results
Hsa_circ_0008673 level was increased in BC tissues and cells. Hsa_circ_0008673 silencing
repressed BC cell growth, metastasis and angiogenesis, as well as hampered BC tumor
growth. Hsa_circ_0008673 acted as miR-578 sponge, and miR-578 targeted GINS4. Furthermore,
hsa_circ_0008673 modulated GINS4 expression through sponging miR-578. Additionally,
miR-578 inhibitor or GINS4 overexpression could reverse the inhibitory effect of hsa_circ_0008673
silencing on BC cell progression.
Conclusion
Hsa_circ_0008673 might promote BC progression via modulating miR-578/GINS4 pathway.
Keywords
Abbreviations:
circRNAs (circular RNAs), BC (breast cancer), miRNA (microRNA), GINS4 (GINS complex subunit 4), qRT-PCR (quantitative real-time PCR)To read this article in full you will need to make a payment
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Article info
Publication history
Published online: December 22, 2022
Accepted:
December 19,
2022
Received in revised form:
November 15,
2022
Received:
March 28,
2022
Identification
Copyright
© 2022 Elsevier Inc. All rights reserved.
