Evidence map›Paper›PMID 30320499›Full record

ArticleJournal of cellular and molecular medicine2018

Functional role of RRS1 in breast cancer cell proliferation.

Jinlian Song, Zhongliang Ma, Yanan Hua, Junting Xu, Ning Li, Chuanxia Ju, Lin Hou

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

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  13. Genomic gain ofScience advances · 2021
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  20. Functional role of RRS1 in breast cancer cell proliferation.Journal of cellular and molecular medicine · 2018
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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

7 authors at 1 institution in 1 country.

Jinlian SongDepartment of Laboratory, The Affiliated Women and Children's Hospital of Qingdao University, Qingdao University, Qingdao, Shandong, China.
Zhongliang MaDepartment of Breast Surgery, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, Shandong, China.
Yanan HuaDepartment of Biochemistry, Medical College, Qingdao University, Qingdao, Shandong, China.
Junting XuDepartment of Biochemistry, Medical College, Qingdao University, Qingdao, Shandong, China.
Ning LiDepartment of Biochemistry, Medical College, Qingdao University, Qingdao, Shandong, China.
Chuanxia JuDepartment of Pharmacology, Qingdao University School of Pharmacy, Qingdao, Shandong, China.
Lin HouDepartment of Biochemistry, Medical College, Qingdao University, Qingdao, Shandong, China.ORCID 0000-0002-6811-2821
Qingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RRS1 (human regulator of ribosome synthesis 1), an essential nuclear protein involved in ribosome biogenesis, is overexpressed in some human cancers, yet its role in breast cancer remains unclear. Here, we report a functional analysis of RRS1 in breast cancer and its likely mechanism. Immunohistochemistry (IHC) and RT-qPCR analyses indicated that RRS1 was commonly overexpressed in breast cancer tissues. The copy numbers of RRS1 were higher in tumours compared with those for normal tissues. And there was a significant correlation between copy number and mRNA expression. In addition, RRS1 overexpression was significantly correlated with lymph node metastasis and poor survival. RRS1 mRNA and protein levels were also significantly increased in a panel of human breast cancer cell lines. RRS1 knockdown inhibited proliferation and induced apoptosis and cell cycle arrest in all three cell lines. Furthermore, RRS1 knockdown suppressed the tumour formation and growth of MDA-MB-231 cells in nude mice. Additionally, RRS1 knockdown activated p53 and p21 in MCF-7 cells. A marked increase in the quantity of ribosome-free RPL11 was detected by Western blot. Moreover, co-immunoprecipitation (CoIP) experiments showed that RRS1 knockdown activated p53 by facilitating the direct contact of MDM2 and RPL11/RPL5. Taken together, our results suggest that RRS1 may contribute to breast cancer proliferation through RPL11/MDM2-mediated p53 activation. Therefore, RRS1 may be a promising target for breast cancer therapy.

Indexed as

AnimalsApoptosisBreast NeoplasmsCell Cycle CheckpointsCell ProliferationFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMCF-7 CellsMiceNuclear ProteinsProto-Oncogene Proteins c-mdm2RNA-Binding ProteinsTumor Suppressor Protein p53Nuclear ProteinsProto-Oncogene Proteins c-mdm2RNA-Binding ProteinsRRS1 protein, humanTrp53 protein, mouseTumor Suppressor Protein p53breast cancerp53proliferationRPL11/MDM2RRS1 gene

Identifiers

PMID30320499
PMCPMC6237566
OpenAlexW2896775320

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.