CDCA4, a downstream gene of the Nrf2 signaling pathway, regulates cell proliferation and apoptosis in the MCF‑7/ADM human breast cancer cell line

Xu,Yuju; Wu,Xianghua; Li,Fengxi; Huang,Daolai; Zhu,Wenxiang

doi:10.3892/mmr.2017.8095

CDCA4, a downstream gene of the Nrf2 signaling pathway, regulates cell proliferation and apoptosis in the MCF‑7/ADM human breast cancer cell line

Authors:
- Yuju Xu
- Xianghua Wu
- Fengxi Li
- Daolai Huang
- Wenxiang Zhu
View Affiliations

Affiliations: Department of Gastrointestinal Gland Surgery, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China
Published online on: November 15, 2017 https://doi.org/10.3892/mmr.2017.8095
Pages: 1507-1512
Copyright: © Xu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )

Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )

Cited By (CrossRef): 0 citations Loading Articles...

Abstract

The present study aimed to examine the effect of RNA interference targeting cell division cycle‑associated protein 4 (CDCA4) on the proliferation and apoptosis of the MCF‑7/ADR' human breast cancer cell line. CDCA4 has been shown to have a unique role in regulating cell cycle. In the present study, the expression of CDCA4 was suppressed by CDCA4‑specific short hairpin (sh)RNA transfection of the human breast cancer cells, following which changes in the proliferation and apoptosis of the CDCA4‑knockdown cells were compared with those of control shRNA‑transfected cells. The results confirmed that CDCA4 RNA interference reduced the percentage of human breast cancer cells to <50%. In addition, RNA interference of CDCA4 resulted in a significant increase in the apoptotic rate of cells. Taken together, these results suggested that CDCA4 enhanced proliferation and reduced apoptosis in the MCF‑7/ADM human breast cancer cells in vitro.

View Figures

View References

1	Abdullah JM, Jing X, Spassov DS, Nachtman RG and Jurecic R: Cloning and characterization of Hepp, a novel gene expressed preferentially in hematopoietic progenitors and mature blood cells. Blood Cells Mol Dis. 27:667–676. 2001. View Article : Google Scholar
2	Walker MG: Drug target discovery by gene expression analysis: Cell cycle genes. Curr Cancer Drug Targets. 1:73–83. 2001. View Article : Google Scholar
3	Lai IL, Wang SY, Yao YL and Yang WM: Transcriptional and subcellular regulation of the TRIP-Br family. Gene. 388:102–109. 2007. View Article : Google Scholar
4	Watanabe-Fukunaga R, Iida S, Shimizu Y, Nagata S and Fukunaga R: SEI family of nuclear factors regulates p53-dependent transcriptional activation. Genes Cells. 10:851–860. 2005. View Article : Google Scholar
5	Cheong JK, Gunaratnam L, Zang ZJ, Yang CM, Sun X, Nasr SL, Sim KG, Peh BK, Rashid SB, Bonventre JV, et al: TRIP-Br2 promotes oncogenesis in nude mice and is frequently overexpressed in multiple human tumors. J Transl Med. 7:82009. View Article : Google Scholar :
6	Tang DJ, Hu L, Xie D, Wu QL, Fang Y, Zeng Y, Sham JS and Guan XY: Oncogenic transformation by SEI-1 is associated with chromosomal instability. Cancer Res. 65:6504–6508. 2005. View Article : Google Scholar
7	Hsu SI, Yang CM, Sim KG, Hentschel DM, O'Leary E and Bonventre JV: TRIP-Br: A novel family of PHD zinc finger- and bromodomain-interacting proteins that regulate the transcriptional activity of E2F-1/DP-1. EMBO J. 20:2273–2285. 2001. View Article : Google Scholar :
8	Li C, Jung S, Lee S, Jeong D, Yang Y, Kim KI, Lim JS, Cheon CI, Kim C, Kang YS and Lee MS: Nutrient/serum starvation derived TRIP-Br3 down-regulation accelerates apoptosis by destabilizing XIAP. Oncotarget. 6:7522–7535. 2015. View Article : Google Scholar :
9	Hong SW, Kim CJ, Park WS, Shin JS, Lee SD, Ko SG, Jung SI, Park IC, An SK, Lee WK, et al: p34SEI-1 inhibits apoptosis through the stabilization of the X-linked inhibitor of apoptosis protein: p34SEI-1 as a novel target for anti-breast cancer strategies. Cancer Res. 69:741–746. 2009. View Article : Google Scholar
10	Hayashi R, Goto Y, Ikeda R, Yokoyama KK and Yoshida K: CDCA4 is an E2F transcription factor family-induced nuclear factor that regulates E2F-dependent transcriptional activation and cell proliferation. J Biol Chem. 281:35633–35648. 2006. View Article : Google Scholar
11	Tategu M, Nakagawa H, Hayashi R and Yoshida K: Transcriptional co-factor CDCA4 participates in the regulation of JUN oncogene expression. Biochimie. 90:1515–1522. 2008. View Article : Google Scholar
12	Lee SL, Hong SW, Shin JS, Kim JS, Ko SG, Hong NJ, Kim DJ, Lee WJ, Jin DH and Lee MS: p34SEI-1 inhibits doxorubicin-induced senescence through a pathway mediated by protein kinase C-delta and c-Jun-NH2-kinase 1 activation in human breast cancer MCF7 cells. Mol Cancer Res. 7:1845–1853. 2009. View Article : Google Scholar
13	Alderman C, Sehlaoui A, Xiao Z and Yang Y: MicroRNA-15a inhibits the growth and invasiveness of malignant melanoma and directly targets on CDCA4 gene. Tumour Biol. 37:13941–13950. 2016. View Article : Google Scholar
14	Wang XJ, Sun Z, Villeneuve NF, Zhang S, Zhao F, Li Y, Chen W, Yi X, Zheng W, Wondrak GT, et al: Nrf2 enhances resistance of cancer cells to chemotherapeutic drugs, the dark side of Nrf2. Carcinogenesis. 29:1235–1243. 2008. View Article : Google Scholar :
15	Livak KJ and Scmittgen TD: Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) method. Methods. 25:402–408. 2001. View Article : Google Scholar
16	Romond EH, Perez EA, Bryant J, Suman VJ, Geyer CE Jr, Davidson NE, Tan-Chiu E, Martino S, Paik S, Kaufman PA, et al: Trastuzumab plus adjuvant chemotherapy for operable HER2-positive breast cancer. N Engl J Med. 353:1673–1684. 2005. View Article : Google Scholar
17	Wang L, Zhu G, Li Q, Li Y, Xu X, He D and Zeng C: The spindle function of CDCA4. Cell Motil Cytoskel. 65:581–593. 2008. View Article : Google Scholar