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Hsa_circRNA_102229 facilitates the progression of triple‐negative breast cancer via regulating the miR‐152‐3p/PFTK1 pathway
Author(s) -
Du Chuang,
Zhang Jianhua,
Zhang Linfeng,
Zhang Yingying,
Wang Yan,
Li Jingruo
Publication year - 2021
Publication title -
the journal of gene medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.689
H-Index - 91
eISSN - 1521-2254
pISSN - 1099-498X
DOI - 10.1002/jgm.3365
Subject(s) - triple negative breast cancer , cancer research , gene knockdown , flow cytometry , microrna , carcinogenesis , metastasis , chemistry , breast cancer , biology , cancer , microbiology and biotechnology , apoptosis , gene , biochemistry , genetics
Background Increasing evidence has suggested that circular RNAs (circRNAs) may act as an important regulatory factor in tumor progression. However, how circRNAs exert their functions in triple‐negative breast cancer (TNBC) remains not clearly understood. Methods First, circRNA microarrays were conducted to identify aberrantly expressed circRNAs in TNBC tissues. Kaplan–Meier survival analysis was conducted to calculate the correlation between the level of hsa_circRNA_102229 and outcomes of patients with TNBC. The effect of hsa_circRNA_102229 and serine/threonine‐protein kinase PFTAIRE 1 (PFTK1) on TNBC cells was clarified by cell counting kit‐8, transwell and wound healing assays, as well as by a flow cytometry. The molecular mechanism of hsa_circRNA_102229 was clarified through bioinformatics, a dual‐luciferase reporter assay, western blotting, fluorescence in situ hybridization and real‐time polymerase chain reaction. Tumor xenograft experiments were performed to analyze growth and metastasis of TNBC in vivo . Results In TNBC tissues and cells, hsa_circ_102229 was remarkably up‐regulated. Patients with TNBC presenting high hsa_circ_102229 exhibited poor prognosis. Moreover, hsa_circ_102229 could promote the migration, proliferation and invasion, whereas it inhibited the apoptosis of TNBC cells. Furthermore, hsa_circ_102229 directly targeted miR‐152‐3p and could regulate the expression of PFTK1 by targeting miR‐152‐3p. Rescue assays suggested that hsa_circ_102229 may exert its function in TNBC cells by regulating PFTK1. Additionally, knockdown of hsa_circ_102229 slowed down TNBC tumorigenesis and lung metastasis in a tumor xenograft animal model. Conclusions Hsa_circ_102229 might serve as a competing endogenous RNA (ceRNA) to modulate PFTK1 expression via regulating miR‐152‐3p to affect the functions of TNBC cells. Hsa_circ_102229 acts as a newly discovered biomarker for TNBC treatment.