Silencing cyclin-dependent kinase inhibitor 3 inhibits the migration of breast cancer cell lines Retraction in /10.3892/mmr.2023.13075

Deng,Miao; Wang,Jianguang; Chen,Yanbin; Zhang,Like; Xie,Gangqiang; Liu,Qipeng; Zhang,Ting; Yuan,Pengfei; Liu,Dechun

doi:10.3892/mmr.2016.5401

Silencing cyclin-dependent kinase inhibitor 3 inhibits the migration of breast cancer cell lines

Retraction in: /10.3892/mmr.2023.13075

Authors:
- Miao Deng
- Jianguang Wang
- Yanbin Chen
- Like Zhang
- Gangqiang Xie
- Qipeng Liu
- Ting Zhang
- Pengfei Yuan
- Dechun Liu
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Affiliations: Department of Breast Surgery, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China
Published online on: June 14, 2016 https://doi.org/10.3892/mmr.2016.5401
Pages: 1523-1530
Copyright: © Deng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Cyclin-dependent kinase inhibitor 3 (CDKN3) belongs to the dual-specificity protein phosphatase family, which is hypothesized to regulate cell cycle progression in tumor cells. However, whether CDKN3 is a potential therapeutic target for breast cancer remains to be elucidated. The present in vitro study aimed to investigate the potential roles of CDKN3 in breast cancer. Breast cancer cell lines were used to detect CDKN3 expression, and CDKN3 expression was silenced to investigate its role in cell apoptosis, cell cycle arrest and migration. The underlying mechanisms were screened by detecting proliferating cell nuclear antigen (PCNA), Ras homolog gene family, member A (RhoA), vimentin, B‑cell lymphoma 2 (Bcl‑2) and Bcl‑2‑associated X protein (Bax) expression. CDKN3 was highly expressed in MCF‑7 and BT474 cell lines. The silencing of CDKN3 in MCF‑7 and BT474 cell lines promoted cell apoptosis, induced G1 phase cell cycle arrest and inhibited cell migration. The expression levels of PCNA, RhoA, vimentin and Bcl‑2 were downregulated following CDKN3 silencing. Conversely, Bax expression was increased, as compared with the vehicle control. These results suggest that CDKN3 acts as an oncogene during breast cancer progression. The in vitro silencing of CDKN3 promoted apoptosis, induced G1 phase cell cycle arrest and inhibited cell migration. Possible mechanisms are associated with the regulation of PCNA, Bcl‑2, vimentin, RhoA and Bax expression. CDKN3 may therefore be considered a potential target for the treatment of breast cancer.

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