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Upregulation of circ-UBAP2 predicts poor prognosis and promotes triple-negative breast cancer progression through the miR-661/MTA1 pathway

Journal Article · · Biochemical and Biophysical Research Communications
; ; ; ; ;  [1];  [2]; ; ;  [1]
  1. Department of Clinical Medicine, Peihua University, Xi'an, 710125 (China)
  2. Department of Spine Surgery, Honghui Hospital, Xi'an Jiaotong University, 710054 (China)
Highlights: • circ-UBAP2 is significantly up-regulated in TNBC and predicts poor prognosis. • Knockdown of circ-UBAP2 remarkably inhibits TNBC progression both in vitro and in vivo. • circ-UBAP2 exerts its oncogenic effect via miR-661/MTA1 axis in TNBC. Recently, a large number of studies have shown that circular RNA (circRNA) is involved in the development and progression of human cancer. However, its role in triple-negative breast cancer (TNBC) remains largely unknown. In this study, a novel circRNA, circ-UBAP2 (hsa{sub c}irc{sub 0}001846), was shown to be markedly upregulated in TNBC. Moreover, high circ-UBAP2 expression was closely associated with larger tumour size (p = 0.003), advanced TNM stage (p = 0.005), lymph node metastasis (p = 0.002), and unfavourable prognosis (p = 0.0256). Functionally, lentivirus-mediated stable knockdown of circ-UBAP2 dramatically weakened the ability of TNBC cells to proliferate and migrate and induced apoptosis in vitro and in vivo. Regarding the mechanism, we found that circ-UBAP2 was mainly observed in the cytoplasm and was capable of sponging miRNA-661 to increase the expression of the oncogene MTA1. Additionally, silencing of miRNA-661 or overexpression of MTA1 could partially rescue the attenuated malignant phenotype caused by circ-UBAP2 knockdown. Taken together, our data reveal that circ-UBAP2 plays a vital regulatory role in TNBC via the miR-661/MTA1 axis and may serve as a promising therapeutic target for TNBC patients.
OSTI ID:
23134101
Journal Information:
Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 4 Vol. 505; ISSN BBRCA9; ISSN 0006-291X
Country of Publication:
United States
Language:
English

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