Evidence map›Paper›PMID 32541902›Full record

ArticleCell death & disease2020

Oncogene PRR14 promotes breast cancer through activation of PI3K signal pathway and inhibition of CHEK2 pathway.

Xiaolei Ren, Meijun Long, Zhihong Li, Boda Wu, Tao Jin, Chao Tu, Lin Qi, Mei Yang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

11 citing papers in PubMed, 13 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

8 authors at 3 institutions in 1 country.

Xiaolei Ren *Department of Orthopedics, The Second Xiangya Hospital, Central South University, Changsha, China.
Meijun Long *Breast Cancer Center, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Zhihong LiDepartment of Orthopedics, The Second Xiangya Hospital, Central South University, Changsha, China.
Boda WuDepartment of Medical Genetics, The Second Xiangya Hospital, Central South University, Changsha, China.
Tao JinDepartment of Medical Genetics, The Second Xiangya Hospital, Central South University, Changsha, China.
Chao TuDepartment of Orthopedics, The Second Xiangya Hospital, Central South University, Changsha, China.
Lin QiDepartment of Orthopedics, The Second Xiangya Hospital, Central South University, Changsha, China.
Mei YangDepartment of Orthopedics, The Second Xiangya Hospital, Central South University, Changsha, China. yangmei23@csu.edu.cn.
Central South University · CNSecond Xiangya Hospital of Central South University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear envelope component PRR14 has been detected to be upregulated in varieties of cancers, especially in breast cancer. But its role in breast carcinogenesis is poorly understood. In this study, we show PRR14 contributes to breast carcinogenesis mainly through overexpression, which derives from elevated transcription and gene amplification. Increased PRR14 expression promotes breast cancer cell proliferation and tumor formation. Biochemical analysis reveals, in addition to previously reported activation of PI3-kinase/Akt/mTOR pathway, PRR14 overexpression regulates cell cycle in breast cancer by inhibiting CHEK2's activation, followed with the deregulation of DNA damage pathway. In correspondence, CHEK2 and PRR14 show opposite impact on breast cancer patients receiving chemotherapy. Collectively, our study is the first to document the oncogenetic role of PRR14 in breast cancer, which protects cells from apoptosis and stimulates proliferation by activating the PI3-kinase/Akt/mTOR pathway and inhibiting the CHEK2 pathway. Both of these pathways are of great influence in breast cancer and PRR14 appears to be their novel interacting node, which renders patients more resistance to chemotherapy and provides a potential therapeutic target in breast cancer.

Indexed as

Breast NeoplasmsCheckpoint Kinase 2Chromosomal Proteins, Non-HistoneFemaleHumansPhosphatidylinositol 3-KinasesSignal TransductionCheckpoint Kinase 2CHEK2 protein, humanChromosomal Proteins, Non-HistonePhosphatidylinositol 3-KinasesPRR14 protein, human

Identifiers

PMID32541902
PMCPMC7296039
OpenAlexW3034403869

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.