Publication: The circCDK17/miR-122-5p/ASF1B axis regulates the progression of cervical cancer
Authors
Qiu, Fang ; Ou, Dafen ; Tan, Hanxing ; Gao, Yan ; Z, Dan
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-18-527
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info:eu-repo/semantics/article
Description
Abstract
Background. Cervical cancer (CC) ranks
fourth in terms of incidence and fourth in mortality
overall in women worldwide. Circular RNAs
(circRNAs) have been shown to be involved in the
development of CC. However, the function of circRNA
cyclin dependent kinase 17 (circCDK17, hsa_circ_
0002762) in CC pathogenesis has not been studied.
Methods. Quantitative real-time polymerase chain
reaction (qRT-PCR) was used to detect the expression of
related genes. MTT, thymidine analog 5-ethynyl-2’-
deoxyuridine (EdU), flow cytometry, transwell and
wound-healing assays were designed to analyze cell
proliferation, cell cycle progression, migration and
invasion, respectively. Western blot was utilized to
examine the protein levels of Cyclin D1, E-cadherin and
Vimentin. The relationship between miR-122-5p and
circCDK17 or ASF1B was verified by dual-luciferase
reporter assay. The xenograft model was established to
study the role of circCDK17 in vivo.
Results. CircCDK17 and anti-silencing function 1B
histone chaperone (ASF1B) were highly expressed in
CC tissues and cells. Silencing circCDK17 reduced the
proliferation, migration and invasion of CC cells. MiR122-5p was a target of circCDK17. Silencing
circCDK17 inhibited the malignant behaviors of CC
cells by releasing miR-122-5p. Moreover, ASF1B was a
target of miR-122-5p. Overexpression of ASF1B
partially restored the inhibitory effects of circCDK17
silencing on cell proliferation, migration and invasion.
Animal experiments confirmed the anti-tumor effect of
circCDK17 knockdown in vivo.
Conclusion. Our study demonstrates that circCDK17
regulates the expression of ASF1B by miR-122-5p
competition and thus promotes the development of CC,
providing a novel targeted therapy for CC.
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Citation
Histology and Histopathology Vol. 38, nº3 (2023)
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