Evidence map›Paper›PMID 38474562›Full record

ArticleMolecules (Basel, Switzerland)2024

Regulator of Ribosome Synthesis 1 (RRS1) Stabilizes GRP78 and Promotes Breast Cancer Progression.

Wenjing Sun, Junying Song, Qinglan Wu, Lin Deng, Tenglong Zhang, Li Zhang, Yanan Hua, Yi Cao, Lin Hou

Abstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

9 authors.

Wenjing SunDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Qingdao University, Qingdao 266011, China.
Junying SongDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Qingdao University, Qingdao 266011, China.
Qinglan WuDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Qingdao University, Qingdao 266011, China.
Lin DengWanzhou District Center for Disease Control, Chongqing 404100, China.
Tenglong ZhangDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Qingdao University, Qingdao 266011, China.
Li ZhangExperimental Center for Undergraduates of Pharmacy, School of Pharmacy, Qingdao University, Qingdao 266011, China.
Yanan HuaChongqing Key Laboratory of Sichuan-Chongqing Co-Construction for Diagnosis and Treatment of Infectious Diseases Integrated Traditional Chinese and Western Medicine, College of Medical Technology, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, China.
Yi CaoDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Qingdao University, Qingdao 266011, China.
Lin HouDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Qingdao University, Qingdao 266011, China.

Funding

Natural Science Fundation of Shandong Province ZR2023MH122Natural Science Fundation of Sichuan Province 2022NSFSC0733Shandong Province Science and Technology and Health Development Plan Project 202102021147Shandong Province Traditional Chinese Medicine Science and Technology Project 2021Z196the National Natural Science Foundation of China 81472542
6 · The paper itself

Abstract

Regulator of ribosome synthesis 1 (RRS1), a crucial regulatory factor in ribosome biogenesis, exerts a remarkable impact on the progression of breast cancer (BC). However, the exact mechanisms and pathways have not yet been fully elucidated. To investigate the impact of RRS1 on BC growth and metastasis, along with its underlying mechanisms. We discovered that RRS1 is overexpressed in BC tissues and cell lines. This study aims to regulate the level of RRS1 through lentiviral transfection technology to explore its potential function in BC cells. Knockdown of RRS1 resulted in the inhibition of cell proliferation, invasion, and migration, whereas overexpression had the opposite effects. We firstly identified the interaction between RRS1 and Glucose-Regulated Protein 78 (GRP78) using Co-immunoprecipitation (Co-IP) combined with mass spectrometry analysis, providing evidences of co-localization and positive regulation between RRS1 and GRP78. We observed that RRS1 inhibited the degradation of GRP78 through the ubiquitin-proteasome pathway, resulting in the stabilization of GRP78. In addition, our findings suggested that RRS1 promoted BC progression by activating the GRP78-mediated phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. In conclusion, this newly discovered RRS1/GRP78 signaling axis provides a molecular and theoretical basis for further exploring the mechanisms of breast cancer invasion and metastasis.

Indexed as

Breast NeoplasmsCell Line, TumorCell ProliferationEndoplasmic Reticulum Chaperone BiPFemaleHumansPhosphatidylinositol 3-KinasesRibosomesRNA-Binding ProteinsEndoplasmic Reticulum Chaperone BiPPhosphatidylinositol 3-KinasesRNA-Binding ProteinsRRS1 protein, humanbreast cancerGRP78interactionRRS1

Identifiers

PMID38474562
PMCPMC10934892

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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.