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Research Paper|Volume 13, Issue 3|pp 4157—4181

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

Pin-Shern Chen1, Hui-Ping Hsu2, Nam Nhut Phan3, Meng-Chi Yen4,5, Feng-Wei Chen6, Yu-Wei Liu1, Fang-Ping Lin1, Sheng-Yao Feng1, Tsung-Lin Cheng7,8,9,10, Pei-Hsiang Yeh1, Hany A. Omar11,12,13, Zhengda Sun14, Jia-Zhen Jiang15, Yi-Shin Chan16, Ming-Derg Lai6, Chih-Yang Wang16,17, Jui-Hsiang Hung1,10
  • 1Department of Biotechnology, Chia Nan University of Pharmacy and Science, Tainan 70101, Taiwan, Republic of China
  • 2Department of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan, Republic of China
  • 3NTT Institute of Hi-Technology, Nguyen Tat Thanh University, Ho Chi Minh 700000, Vietnam
  • 4Department of Emergency Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80708, Taiwan, Republic of China
  • 5Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan, Republic of China
  • 6Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan, Republic of China
  • 7Department of Physiology, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan, Republic of China
  • 8Orthopedic Research Center, College of Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80708, Taiwan, Republic of China
  • 9Department of Medical Research, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80708, Taiwan, Republic of China
  • 10Regenerative Medicine and Cell Therapy Research Center, Kaohsiung Medical University, Kaohsiung 80708, Taiwan, Republic of China
  • 11Sharjah Institute for Medical Research and College of Pharmacy, University of Sharjah, Sharjah 27272, United Arab Emirates
  • 12Department of Clinical Sciences, College of Pharmacy, Ajman University, Ajman 23000, United Arab Emirates
  • 13Department of Pharmacology, Faculty of Pharmacy, BeniSuef University, Beni-Suef 62511, Egypt
  • 14Kaiser Permanente, Northern California Regional Laboratories, The Permanente Medical Group, Berkeley, CA 94710, USA
  • 15Emergency Department, Huashan Hospital North, Fudan University, Shanghai 201508, People’s Republic of China
  • 16Graduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan, Republic of China
  • 17PhD Program for Cancer Molecular Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan, Republic of China
* Equal contribution
# Senior author
Received: June 25, 2020Accepted: November 20, 2020Published: January 10, 2021

Copyright: © 2021 Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

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.