Evidence map›Paper›PMID 30177834›Full record

ArticleOncogene2019

A mandatory role of nuclear PAK4-LIFR axis in breast-to-bone metastasis of ERα-positive breast cancer cells.

Yanshu Li, Hongyan Zhang, Yue Zhao, Chunyu Wang, Zhenguo Cheng, Lina Tang, Yunling Gao, Furong Liu, Jiabin Li, Yan Li and 9 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
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  8. Organ-Specificity of Breast Cancer Metastasis.International journal of molecular sciences · 2023
    Review
  9. The role of p21-activated kinase 4 in the progression of oral squamous cell carcinoma by targeting PI3K-AKT signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
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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

19 authors at 3 institutions in 2 countries.

Yanshu LiDepartment of Cell Biology, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, China Medical University, No. 77, Puhe Road, Shenyang North New Area, 110122, Shenyang, Liaoning, China.
Hongyan ZhangDepartment of Cell Biology, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, China Medical University, No. 77, Puhe Road, Shenyang North New Area, 110122, Shenyang, Liaoning, China.
Yue ZhaoDepartment of Cell Biology, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, China Medical University, No. 77, Puhe Road, Shenyang North New Area, 110122, Shenyang, Liaoning, China.
Chunyu WangDepartment of Cell Biology, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, China Medical University, No. 77, Puhe Road, Shenyang North New Area, 110122, Shenyang, Liaoning, China.
Zhenguo ChengDepartment of Cell Biology, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, China Medical University, No. 77, Puhe Road, Shenyang North New Area, 110122, Shenyang, Liaoning, China.
Lina TangDepartment of Cell Biology, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, China Medical University, No. 77, Puhe Road, Shenyang North New Area, 110122, Shenyang, Liaoning, China.
Yunling GaoDepartment of Cell Biology, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, China Medical University, No. 77, Puhe Road, Shenyang North New Area, 110122, Shenyang, Liaoning, China.
Furong LiuDepartment of Cell Biology, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, China Medical University, No. 77, Puhe Road, Shenyang North New Area, 110122, Shenyang, Liaoning, China.
Jiabin LiDepartment of Cell Biology, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, China Medical University, No. 77, Puhe Road, Shenyang North New Area, 110122, Shenyang, Liaoning, China.
Yan LiDepartment of Cell Biology, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, China Medical University, No. 77, Puhe Road, Shenyang North New Area, 110122, Shenyang, Liaoning, China.
Yang LiDepartment of Cell Biology, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, China Medical University, No. 77, Puhe Road, Shenyang North New Area, 110122, Shenyang, Liaoning, China.
Nanxi GengDepartment of Cell Biology, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, China Medical University, No. 77, Puhe Road, Shenyang North New Area, 110122, Shenyang, Liaoning, China.ORCID http://orcid.org/0000-0002-7549-3431
Xue RuiDepartment of Surgical Oncology, The First Hospital of China Medical University, No. 155, North Nanjing Street, Heping District, 110001, Shenyang, Liaoning, China.
Yuee TengDepartment of Medical Oncology, The First Hospital of China Medical University, No. 155, North Nanjing Street, Heping District, 110001, Shenyang, Liaoning, China.
Yunpeng LiuDepartment of Medical Oncology, The First Hospital of China Medical University, No. 155, North Nanjing Street, Heping District, 110001, Shenyang, Liaoning, China.
Liu CaoDepartment of Cell Biology, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, China Medical University, No. 77, Puhe Road, Shenyang North New Area, 110122, Shenyang, Liaoning, China.
Rakesh KumarCancer Research Program, Rajiv Gandhi Centre for Biotechnology, Thiruvananthapuram, 695014, Kerala, India.
Feng JinDepartment of Surgical Oncology, The First Hospital of China Medical University, No. 155, North Nanjing Street, Heping District, 110001, Shenyang, Liaoning, China. jinfeng@cmu.edu.cn.
Feng LiDepartment of Cell Biology, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, China Medical University, No. 77, Puhe Road, Shenyang North New Area, 110122, Shenyang, Liaoning, China. lifeng@cmu.edu.cn.
China Medical University · CNFirst Hospital of China Medical University · CNRajiv Gandhi Centre for Biotechnology · IN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31371424National Natural Science Foundation of China (National Science Foundation of China) 31571457National Natural Science Foundation of China (National Science Foundation of China) 90813038
6 · The paper itself

Abstract

The mechanism of estrogen receptor alpha (ERα)-positive breast cancer-associated bone metastasis is poorly understood. In this article, we report that nuclear p21-activated kinase 4 (nPAK4) is a novel repressor of ERα-mediated transactivation in a 17β-estradiol (E2)-dependent manner and promotes PAK4-ERα axis-mediated bone metastasis by targeting leukemia inhibitory factor receptor (LIFR) in ERα-positive breast cancer. An evaluation of clinical breast cancer samples revealed that nPAK4 is linked to ERα expression and appears to be associated with a poor prognosis in bone metastatic breast cancer. PAK4 bound and co-translocated with ERα from the cytoplasm to the nucleus upon stimulation with E2. nPAK4 enhanced the invasive potential of ERα-positive breast cancer cells in vitro and promoted breast cancer metastasis in vivo. Mechanistically, nPAK4 promoted the metastasis of ERα-positive breast cancer cells by targeting LIFR, a bone metastasis suppressor. Strikingly, the nuclear accumulation of PAK4 might promote aggressive phenotypes, highlighting nPAK4 as a novel predictive biomarker for ERα-positive breast cancer bone metastasis.

Indexed as

AnimalsBiomarkers, TumorBone NeoplasmsBreast NeoplasmsCell NucleusDrosophila melanogasterEstrogen Receptor alphaFemaleHumansLeukemia Inhibitory Factor Receptor alpha SubunitMCF-7 CellsMiceMice, Inbred BALB CNeoplasm InvasivenessNeoplasm MetastasisNeoplasm ProteinsBiomarkers, TumorESR1 protein, humanEstrogen Receptor alphaLeukemia Inhibitory Factor Receptor alpha SubunitLIFR protein, humanNeoplasm Proteinsp21-Activated KinasesPAK4 protein, human

Identifiers

PMID30177834
PMCPMC6367215
OpenAlexW2889777908

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.