Evidence map›Paper›PMID 39370816›Full record

ArticleMolecular medicine reports2024

ETV4‑mediated transcriptional activation of SLC12A5 exacerbates ferroptosis resistance and glucose metabolism reprogramming in breast cancer cells.

Huan Wang, Yanyan Dai, Fengxiang Wang

Abstract read
In one paragraph

Article in Molecular medicine reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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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

3 citing papers in PubMed.

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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.

Huan WangDepartment of Pathology, Wenzhou Central Hospital, Wenzhou, Zhejiang 325000, P.R. China.
Yanyan DaiDepartment of Pathology, Wenzhou Central Hospital, Wenzhou, Zhejiang 325000, P.R. China.
Fengxiang WangDepartment of Pathology, Wenzhou Central Hospital, Wenzhou, Zhejiang 325000, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Solute carrier family 12 member 5 (SLC12A5) is an oncogene in numerous types of cancer, however its function in breast cancer (BC) remains elusive. ETS translocation variant 4 (ETV4) promotes BC. Therefore, the present study aimed to elucidate the role of SLC12A5 in ferroptosis and glucose metabolism in BC cells as well as to understand the underlying mechanism. Analysis of data from the UALCAN database demonstrated expression levels of SLC12A5 in BC and its association with prognosis. Reverse transcription‑quantitative PCR and western blotting were conducted to evaluate the expression levels of SLC12A5 and ETV4 in BC cells. The abilities of BC cells to proliferate, migrate and invade were assessed using Cell Counting Kit‑8, colony formation, wound healing and Transwell assays. Thiobarbituric acid reactive substances assay and a C11 BODIPY 581/591 probe were used to evaluate lipid peroxidation. Ferroptosis resistance was evaluated by the measurement of Fe

Indexed as

Breast NeoplasmsFerroptosisGene Expression Regulation, NeoplasticGlucoseTranscriptional ActivationAdenovirus E1A ProteinsAmino Acid Transport System y+Cell Line, TumorCell MovementCell ProliferationCoenzyme A LigasesFemaleHumansLong-Chain-Fatty-Acid-CoA LigaseMCF-7 CellsMetabolic ReprogrammingAdenovirus E1A ProteinsAmino Acid Transport System y+Coenzyme A LigasesETV4 protein, humanGlucoseLong-Chain-Fatty-Acid-CoA LigasePhospholipid Hydroperoxide Glutathione PeroxidaseProto-Oncogene Proteins c-etsSLC7A11 protein, humanbreast cancerETS translocation variant 4ferroptosisglucose metabolism reprogrammingsolute carrier family 12 member 5

Identifiers

PMID39370816
PMCPMC11465427

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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.