Evidence map›Paper›PMID 31513357›Full record

ArticleMolecular genetics & genomic medicine2019

High expression of PRKDC promotes breast cancer cell growth via p38 MAPK signaling and is associated with poor survival.

Yan Zhang, Wei-Kang Yang, Guo-Ming Wen, Hongping Tang, Chuan-An Wu, Yan-Xia Wu, Zhi-Liang Jing, Min-Shan Tang, Guang-Long Liu, Da-Zhou Li and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular genetics & genomic medicine, 2019. 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
2.1field-weighted citation impact, top 12% 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, 42 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Yan ZhangDepartment of Pathology, Shenzhen Longhua District Maternity & Child Healthcare Hospital, Shenzhen, P.R. China.ORCID 0000-0002-5027-6430
Wei-Kang YangDepartment of Prevention and Health Care, Shenzhen Longhua District Maternity & Child Healthcare Hospital, Shenzhen, P.R. China.
Guo-Ming WenDepartment of Outpatient, Shenzhen Longhua District Maternity & Child Healthcare Hospital, Shenzhen, P.R. China.
Hongping TangDepartment of Pathology, Shenzhen Maternity & Child Healthcare Hospital, Shenzhen, P.R. China.
Chuan-An WuDepartment of Prevention and Health Care, Shenzhen Longhua District Maternity & Child Healthcare Hospital, Shenzhen, P.R. China.
Yan-Xia WuDepartment of Pathology, Nanfang Hospital and School of Basic Medical Sciences, Southern Medical University, Guangzhou, P.R. China.
Zhi-Liang JingDepartment of Pathology, Nanfang Hospital and School of Basic Medical Sciences, Southern Medical University, Guangzhou, P.R. China.
Min-Shan TangDepartment of Pathology, Nanfang Hospital and School of Basic Medical Sciences, Southern Medical University, Guangzhou, P.R. China.
Guang-Long LiuDepartment of Pathology, Nanfang Hospital and School of Basic Medical Sciences, Southern Medical University, Guangzhou, P.R. China.
Da-Zhou LiDepartment of Pathology, Nanfang Hospital and School of Basic Medical Sciences, Southern Medical University, Guangzhou, P.R. China.
Yan-Hua LiDepartment of Pathology, Shenzhen Longhua District Maternity & Child Healthcare Hospital, Shenzhen, P.R. China.
Yong-Jian DengDepartment of Pathology, Nanfang Hospital and School of Basic Medical Sciences, Southern Medical University, Guangzhou, P.R. China.ORCID 0000-0002-9219-9023
Nanfang Hospital · CNShenzhen Maternity and Child Healthcare Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDNA-Dependent Protein Kinase Catalytic Subunit (PRKDC), a key component of the DNA damage repair pathway, is associated with chemotherapy resistance and tumor progression.

methodsHere we analyzed transcriptome data of ~2,000 breast cancer patients and performed functional studies in vitro to investigate the function of PRKDC in breast cancer.

resultsOur results revealed overexpression of PRKDC in multiple breast cancer subtypes. Consistent with patients' data, overexpression of PRKDC was also observed in breast cancer cell lines compared to normal breast epithelial cells. Knockdown of PRKDC in MCF-7 and T47D breast cancer cell lines resulted in proliferation inhibition, reduced colony formation and G2/M cell cycle arrest. Furthermore, we showed that PRKDC knockdown induced proliferation inhibition through activation of p38 MAPK, but not ERK MAPK, signaling pathway in breast cancer cells. Blockage of p38 MAPK signaling could largely rescue proliferation inhibition and cell cycle arrest induced by PRKDC knockdown. Moreover, we analyzed gene expression and clinical data from six independent breast cancer cohorts containing ~1,000 patients. In all cohorts, our results consistently showed that high expression of PRKDC was significantly associated with poor survival in both treated and untreated breast cancer patients.

conclusionTogether, our results suggest that high expression of PRKDC facilitates breast cancer cell growth via regulation of p38 MAPK signaling, and is a prognostic marker for poor survival in breast cancer patients.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisBiomarkers, TumorBreast NeoplasmsCell CycleCell ProliferationDNA-Activated Protein KinaseFemaleFollow-Up StudiesHumansp38 Mitogen-Activated Protein KinasesPrognosisRNA, Small InterferingSurvival RateTumor Cells, CulturedBiomarkers, TumorDNA-Activated Protein Kinasep38 Mitogen-Activated Protein KinasesPRKDC protein, humanRNA, Small Interferingbreast cancercell cyclecell proliferationp38 MAPKPRKDC

Identifiers

PMID31513357
PMCPMC6825841
OpenAlexW2972863033

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.