Evidence map›Paper›PMID 30760381›Full record

ArticleBMB reports2019

PRR11 and SKA2 gene pair is overexpressed and regulated by p53 in breast cancer.

Yitao Wang, Chunxu Zhang, Li Mai, Yulong Niu, Yingxiong Wang, Youquan Bu

Open access · goldAbstract read
In one paragraph

Article in BMB reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed, 36 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

6 authors at 4 institutions in 1 country.

Yitao WangDepartment of Biochemistry and Molecular Biology, Chongqing Medical University, Chongqing 400016, China.
Chunxu ZhangLaboratory of Birth Defects and Related Diseases of Women and Children, West China Second University Hospital, Sichuan University, Chengdu 610000, China.
Li MaiDepartment of Clinical Laboratory, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.
Yulong NiuDepartment of Biochemistry and Molecular Biology, Chongqing Medical University, Chongqing 400016, China.
Yingxiong WangLaboratory of Reproductive Biology, School of Public Health, Chongqing Medical University, Chongqing 400016, China.
Youquan BuDepartment of Biochemistry and Molecular Biology, Chongqing Medical University, Chongqing 400016, China.
Chongqing Medical University · CNChongqing Public Health Medical Center · CNSecond Affiliated Hospital of Chongqing Medical University · CNSichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous study found that two novel cancer-related genes, PRR11 and SKA2, constituted a classic gene pair that was regulated by p53 and NF-Y in lung cancer. However, their role and regulatory mechanism in breast cancer remain elusive. In this study, we found that the expression levels of PRR11 and SKA2 were upregulated and have a negative prognotic value in breast cancer. Loss-of-function experiments showed that RNAi-mediated knockdown of PRR11 and/or SKA2 inhibited proliferation, migration, and invasion of breast cancer cells. Mechanistic experiments revealed that knockdown of PRR11 and/or SKA2 caused dysregulation of several downstream genes, including CDK6, TPM3, and USP12, etc. Luciferase reporter assays demonstrated that wild type p53 significantly repressed the PRR11-SKA2 bidirectional promoter activity, but not NF-Y. Interestingly, NF-Y was only essential for and correlated with the expression of PRR11, but not SKA2. Consistently, adriamycin-induced (ADR) activation of endogenous p53 also caused significant repression of the PRR11 and SKA2 gene pair expression. Notably, breast cancer patients with lower expression levels of either PRR11 or SKA2, along with wild type p53, exhibited better disease-free survival compared to others with p53 mutations and/or higher expression levels of either PRR11 or SKA2. Collectively, our study indicates that the PRR11 and SKA2 transcription unit might be an oncogenic contributor and might serve as a novel diagnostic and therapeutic target in breast cancer. [BMB Reports 2019; 52(2): 157-162].

Indexed as

Breast NeoplasmsCell Line, TumorCell MovementCell ProliferationChromosomal Proteins, Non-HistoneDisease-Free SurvivalFemaleGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateMCF-7 CellsNeoplasm InvasivenessPrognosisPromoter Regions, GeneticProteinsTranscriptional ActivationChromosomal Proteins, Non-HistoneProteinsPRR11 protein, humanSKA2 protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID30760381
PMCPMC6443325
OpenAlexW2916953629

What OpenQuestion holds

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Registered trials

None linked

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.