Evidence map›Paper›PMID 33461170›Full record

ArticleAging2021

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

Pin-Shern Chen, Hui-Ping Hsu, Nam Nhut Phan, Meng-Chi Yen, Feng-Wei Chen, Yu-Wei Liu, Fang-Ping Lin, Sheng-Yao Feng, Tsung-Lin Cheng, Pei-Hsiang Yeh and 7 more

Open access · greenAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 28 citations in OpenAlex.

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  14. CDC167 exhibits potential as a biomarker for airway inflammation in asthma.Mammalian genome : official journal of the International Mammalian Genome Society · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors at 10 institutions in 6 countries.

Pin-Shern ChenDepartment of Biotechnology, Chia Nan University of Pharmacy and Science, Tainan 70101, Taiwan, Republic of China.
Hui-Ping HsuDepartment of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan, Republic of China.
Nam Nhut PhanNTT Institute of Hi-Technology, Nguyen Tat Thanh University, Ho Chi Minh 700000, Vietnam.
Meng-Chi YenDepartment of Emergency Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80708, Taiwan, Republic of China.
Feng-Wei ChenDepartment of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan, Republic of China.
Yu-Wei LiuDepartment of Biotechnology, Chia Nan University of Pharmacy and Science, Tainan 70101, Taiwan, Republic of China.
Fang-Ping LinDepartment of Biotechnology, Chia Nan University of Pharmacy and Science, Tainan 70101, Taiwan, Republic of China.
Sheng-Yao FengDepartment of Biotechnology, Chia Nan University of Pharmacy and Science, Tainan 70101, Taiwan, Republic of China.
Tsung-Lin ChengDepartment of Physiology, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan, Republic of China.
Pei-Hsiang YehDepartment of Biotechnology, Chia Nan University of Pharmacy and Science, Tainan 70101, Taiwan, Republic of China.
Hany A OmarSharjah Institute for Medical Research and College of Pharmacy, University of Sharjah, Sharjah 27272, United Arab Emirates.
Zhengda SunKaiser Permanente, Northern California Regional Laboratories, The Permanente Medical Group, Berkeley, CA 94710, USA.
Jia-Zhen JiangEmergency Department, Huashan Hospital North, Fudan University, Shanghai 201508, People's Republic of China.
Yi-Shin ChanGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan, Republic of China.
Ming-Derg LaiDepartment of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan, Republic of China.
Chih-Yang WangGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan, Republic of China.
Jui-Hsiang HungDepartment of Biotechnology, Chia Nan University of Pharmacy and Science, Tainan 70101, Taiwan, Republic of China.
Chia Nan University of Pharmacy and Science · TWKaohsiung Medical University · TWNational Cheng Kung University · TWTaipei Medical University · TWFudan University · CNKaiser Permanente · USKaohsiung Medical University Chung-Ho Memorial Hospital · TWNational Cheng Kung University Hospital · TWTrường ĐH Nguyễn Tất Thành · VNUniversity of Sharjah · AE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Antineoplastic AgentsBreast NeoplasmsCarboplatinCell CycleCell ProliferationDoxorubicinFemaleFluorouracilGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMCF-7 CellsPaclitaxelRNA, MessengerAntineoplastic AgentsCarboplatinDoxorubicinFluorouracilPaclitaxelRNA, Messengerbioinformaticsbreast cancercell growthcell proliferationcoiled-coil domain-containing protein 167

Identifiers

PMID33461170
PMCPMC7906182
OpenAlexW3121111714

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.