Evidence map›Paper›PMID 35293275›Full record

ArticleBioengineered2022

Ribosomal protein L5 (RPL5)/ E2F transcription factor 1 (E2F1) signaling suppresses breast cancer progression via regulating endoplasmic reticulum stress and autophagy.

Xiaoping Ma, Yan Li, Bing Zhao

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

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  7. Research Progress of Ribosomal Proteins in Reproductive Development.International journal of molecular sciences · 2024
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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

3 authors.

Xiaoping MaBreast Internal Medicine Department, The 3rd Affiliated Teaching Hospital of XinJiang Medical University(Affiliated Tumor Hospital), Urumqi, China.
Yan LiBreast Internal Medicine Department, The 3rd Affiliated Teaching Hospital of XinJiang Medical University(Affiliated Tumor Hospital), Urumqi, China.
Bing ZhaoBreast Internal Medicine Department, The 3rd Affiliated Teaching Hospital of XinJiang Medical University(Affiliated Tumor Hospital), Urumqi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endoplasmic reticulum stress (ERS) is associated with breast cancer progression. However, the potential role of ribosomal protein L5 (RPL5) on ERS in breast cancer remains unclear. This study aimed to determine the role of RPL5/E2F transcription factor 1 (E2F1) in breast cancer. It was found that RPL5 was downregulated in breast cancer cells and tissues. Additionally, overexpression of RPL5 inhibited cell proliferation. Moreover, the levels of ERS and autophagy markers were estimated using western blotting. Overexpression of RPL5 induced ERS and suppressed autophagy. Additionally, RPL5 downregulated E2F1, which was overexpressed in breast cancer cells. However, E2F1 knockdown promoted the transcriptional activation of glucose regulated protein 78 (GRP78), suppressed ERS response, and promoted autophagy. Rescue assays indicated that the effects of RPL5 on ERS and autophagy were abolished by E2F1. Taken together, RPL5 inhibited the growth of breast cancer cells by modulating ERS and autophagy via the regulation of E2F1. These findings suggest that RPL5 has a tumor-suppressive effect in breast cancer.

Indexed as

Breast NeoplasmsEndoplasmic Reticulum StressRibosomal ProteinsApoptosisAutophagyE2F1 Transcription FactorEndoplasmic Reticulum Chaperone BiPFemaleHumansE2F1 protein, humanE2F1 Transcription FactorEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanribosomal protein L5Ribosomal ProteinsautophagyBreast cancerE2F1endoplasmic reticulum stressRPL5

Identifiers

PMID35293275
PMCPMC9161874
OpenAlexW4220743613

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.