Evidence map›Paper›PMID 37626035›Full record

ArticleCell death & disease2023

EIF4A3-mediated circ_0042881 activates the RAS pathway via miR-217/SOS1 axis to facilitate breast cancer progression.

Chenxi Ju, Mingxia Zhou, Dan Du, Chang Wang, Jieqiong Yao, Hongle Li, Yang Luo, Fucheng He, Jing He

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 32 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

9 authors at 4 institutions in 1 country.

Chenxi Ju *Department of Medical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Mingxia Zhou *Department of Gastroenterology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Dan Du *Department of Medical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Chang WangDepartment of Medical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Jieqiong YaoDepartment of Pathology, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, 450014, China.
Hongle LiDepartment of Molecular Pathology, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, 450008, China.
Yang LuoDepartment of Medical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. luoy@cqu.edu.cn.
Fucheng HeDepartment of Medical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. hefucheng@zzu.edu.cn.ORCID 0000-0002-9024-1144
Jing HeDepartment of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. hejing92921@163.com.
First Affiliated Hospital of Zhengzhou University · CNChongqing University · CNSecond Affiliated Hospital of Zhengzhou University · CNZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer (BC) is one of the most frequent cancer-related deaths in women worldwide. Studies have shown the potential impact of circRNAs in multiple human tumorigeneses. Research on the vital signaling pathways and therapeutic targets of circRNAs is indispensable. Here, we aimed to investigate the clinical implications and underlying mechanisms of circ_0042881 in BC. RT-qPCR validated circ_0042881 was notably elevated in BC tissues and plasma, and closely associated with BC clinicopathological features. Functionally, circ_0042881 significantly accelerated the proliferation, migration, and invasion of BC cells in vitro and tumor growth and metastasis in vivo. Mechanistically, circ_0042881 promoted BC progression by sponging miR-217 to relieve its inhibition effect in son of sevenless 1 (SOS1), which further activated RAS protein and initiated downstream signaling cascades, including MEK/ERK pathway and PI3K/AKT pathway. We also demonstrated that treatment of BAY-293, an inhibitor of SOS1 and RAS interaction, attenuated BC progression induced by circ_0042881 overexpression. Furthermore, Eukaryotic initiation factor 4A-III (EIF4A3) could facilitate circ_0042881 circularization. Altogether, we proposed a novel signaling network in which circ_0042881, induced by EIF4A3, influences the process of BC tumorigenesis and metastasis by miR-217/SOS1 axis.

Indexed as

Breast NeoplasmsMicroRNAsCarcinogenesisDEAD-box RNA HelicasesEukaryotic Initiation Factor-4AFemaleHumansNuclear FamilyPhosphatidylinositol 3-KinasesRNA, CircularDEAD-box RNA HelicasesEIF4A3 protein, humanEukaryotic Initiation Factor-4AMicroRNAsMIRN217 microRNA, humanPhosphatidylinositol 3-KinasesRNA, Circular

Identifiers

PMID37626035
PMCPMC10457341
OpenAlexW4386162757

What OpenQuestion holds

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LicenceCC BY
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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.