CCDC167 as a potential therapeutic target and regulator of cell cycle-related networks in breast cancer

According to cancer statistics reported in 2020, breast cancer constitutes 30% of new cancer cases diagnosed in American women. Histological markers of breast cancer are expressions of the estrogen receptor (ER), the progesterone receptor (PR), and human epidermal growth factor receptor (HER)-2. Up...

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Published inAging (Albany, NY.) Vol. 13; no. 3; pp. 4157 - 4181
Main Authors Chen, Pin-Shern, Hsu, Hui-Ping, Phan, Nam Nhut, Yen, Meng-Chi, Chen, Feng-Wei, Liu, Yu-Wei, Lin, Fang-Ping, Feng, Sheng-Yao, Cheng, Tsung-Lin, Yeh, Pei-Hsiang, Omar, Hany A, Sun, Zhengda, Jiang, Jia-Zhen, Chan, Yi-Shin, Lai, Ming-Derg, Wang, Chih-Yang, Hung, Jui-Hsiang
Format Journal Article
LanguageEnglish
Published United States Impact Journals 15.02.2021
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Summary:According to cancer statistics reported in 2020, breast cancer constitutes 30% of new cancer cases diagnosed in American women. Histological markers of breast cancer are expressions of the estrogen receptor (ER), the progesterone receptor (PR), and human epidermal growth factor receptor (HER)-2. Up to 80% of breast cancers are grouped as ER-positive, which implies a crucial role for estrogen in breast cancer development. Therefore, identifying potential therapeutic targets and investigating their downstream pathways and networks are extremely important for drug development in these patients. Through high-throughput technology and bioinformatics screening, we revealed that coiled-coil domain-containing protein 167 (CCDC167) was upregulated in different types of tumors; however, the role of CCDC167 in the development of breast cancer still remains unclear. Integrating many kinds of databases including ONCOMINE, MetaCore, IPA, and Kaplan-Meier Plotter, we found that high expression levels of CCDC167 predicted poor prognoses of breast cancer patients. Knockdown of CCDC167 attenuated aggressive breast cancer growth and proliferation. We also demonstrated that treatment with fluorouracil, carboplatin, paclitaxel, and doxorubicin resulted in decreased expression of CCDC167 and suppressed growth of MCF-7 cells. Collectively, these findings suggest that CCDC167 has high potential as a therapeutic target for breast cancer.
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Equal contribution
Senior author
ISSN:1945-4589
1945-4589
DOI:10.18632/aging.202382