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RCC2 Expression Stimulates ER-Positive Breast Tumorigenesis
Joint Authors
Chang, Xiaotian
Wang, Weiqi
Xu, Bing
Zhang, Zhaoxu
Fang, Kehua
Source
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-13, 13 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-05-23
Country of Publication
Egypt
No. of Pages
13
Main Subjects
Abstract EN
Objective.
Regulator of chromosome condensation 2 (RCC2) has been reported to be involved in the regulation of cell cleavage.
This study investigated the effect of RCC2 expression on breast tumorigenesis.
Methods.
MCF-7 cells originating from estrogen receptor-positive (ER+) breast cancer were transfected with anti-RCC2 siRNA or RCC2-expressing plasmids.
Cell proliferation, apoptosis, migration, and cytokine production in the transfected cells were examined using the CCK-8 assay, wound healing assay, and flow cytometry, respectively.
PCR array was used to investigate the tumorigenic pathway of RCC2 in MCF-7 cells transfected with the anti-RCC2 siRNA.
MCF-7 cells were also transfected with lentivirus-containing anti-RCC2 short hairpin RNA and were injected into BALB/c nude mice to generate tumor-bearing mice.
Tumor growth in the mouse model was examined using magnetic resonance imaging by diffusion-weighted imaging analysis.
Results.
Western blotting and immunohistochemistry detected significantly increased expression of RCC2 in ER + breast tumor tissues compared with breast fibroadenoma samples.
Inhibiting RCC2 expression decreased cell migration and stimulated apoptosis in MCF-7 cells, while overexpressing RCC2 stimulated cell migration and inhibited apoptosis.
The inhibition of RCC2 expression significantly decreased breast tumor growth and IL-6 levels in the tumor-bearing mice.
PCR array demonstrated that inhibiting RCC2 expression significantly decreased the expression of IGF1 and TWIST1, two well-known tumor-enhancing genes, in MCF-7 cells; conversely, overexpressing RCC2 increased the expression levels of these two genes in the transfected cells.
This result was verified in the mouse model following inhibition of RCC2 expression in MCF-7 cells.
Additionally, estradiol-17β suppressed MCF-7 cell apoptosis, stimulated cell proliferation and cell migration, and increased RCC2, IGF1, and TWIST1 expression.
The siRNA-mediated inhibition of RCC2 expression alleviated the inhibitory effects of estrogen on apoptosis in MCF-7 cells, while overexpressing RCC2 enhanced the estrogen-driven inhibition of apoptosis.
Modifying RCC2 expression had no impact on MCF-7 cell proliferation in the presence or absence of estradiol-17β.
Conclusions.
Our results suggest that estrogen-induced RCC2 expression prompts IGF1, TWIST1, and IL-6 expression, stimulates cell migration, and inhibits apoptosis to contribute to ER + breast tumorigenesis.
American Psychological Association (APA)
Wang, Weiqi& Xu, Bing& Zhang, Zhaoxu& Fang, Kehua& Chang, Xiaotian. 2020. RCC2 Expression Stimulates ER-Positive Breast Tumorigenesis. Journal of Oncology،Vol. 2020, no. 2020, pp.1-13.
https://search.emarefa.net/detail/BIM-1188997
Modern Language Association (MLA)
Wang, Weiqi…[et al.]. RCC2 Expression Stimulates ER-Positive Breast Tumorigenesis. Journal of Oncology No. 2020 (2020), pp.1-13.
https://search.emarefa.net/detail/BIM-1188997
American Medical Association (AMA)
Wang, Weiqi& Xu, Bing& Zhang, Zhaoxu& Fang, Kehua& Chang, Xiaotian. RCC2 Expression Stimulates ER-Positive Breast Tumorigenesis. Journal of Oncology. 2020. Vol. 2020, no. 2020, pp.1-13.
https://search.emarefa.net/detail/BIM-1188997
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1188997