Knockdown of cell division cycle‑associated protein 4 expression inhibits proliferation of triple negative breast cancer MDA‑MB‑231 cells in vitro and in vivo

Pang,Sen; Xu,Yuju; Chen,Jun; Li,Guibin; Huang,Jingle; Wu,Xianghua

doi:10.3892/ol.2019.10077

Knockdown of cell division cycle‑associated protein 4 expression inhibits proliferation of triple negative breast cancer MDA‑MB‑231 cells in vitro and in vivo

Authors:
- Sen Pang
- Yuju Xu
- Jun Chen
- Guibin Li
- Jingle Huang
- Xianghua Wu
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Affiliations: Department of Gastrointestinal and Gland Surgery, The First Affiliated Hospital, Guangxi Medical University, Nanning, Guangxi 530021, P.R. China
Published online on: February 26, 2019 https://doi.org/10.3892/ol.2019.10077
Pages: 4393-4400
Copyright: © Pang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Cell division cycle‑associated protein 4 (CDCA4), also known as SEI‑3/hematopoietic progenitor protein, is a target gene of transcription factor E2F and represses E2F‑dependent transcriptional activation and cell proliferation. The present study investigated the effects of CDCA4 knockdown on the regulation of triple negative breast cancer (TNBC) cell proliferation in vitro and in vivo. Human TNBC MDA‑MB‑231 cells were subjected to CDCA4 expression knockdown using a lentiviral vector carrying CDCA4 or a negative control short hairpin RNA, and reverse transcription‑quantitative polymerase chain reaction, MTT cell viability, cell growth, flow cytometric apoptosis, cell cycle and nude mouse tumorigenesis assays were conducted. The knockdown of CDCA4 expression effectively inhibited the growth of MDA‑MB‑231 cells by promoting apoptosis in vitro. Additionally, CDCA4 expression knockdown suppressed nude mouse tumor cell xenograft formation and growth in vivo. In conclusion, the data from the present study supported the hypothesis that CDCA4 may be involved in regulating human TNBC progression, and that targeting CDCA4 expression could be useful as a novel strategy in future TNBC treatment.

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