Evidence map›Paper›PMID 33846793›Full record

ArticleOncology reports2021

CREB stimulates GPX4 transcription to inhibit ferroptosis in lung adenocarcinoma.

Zhixian Wang, Xiao Zhang, Xiaoting Tian, Yueyue Yang, Lifang Ma, Jiayi Wang, Yongchun Yu

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

Article in Oncology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
16.9field-weighted citation impact, top 1% 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

64 citing papers in PubMed, 128 citations in OpenAlex.

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  17. GATA1 activates HSD17B6 to improve efficiency of cisplatin in lung adenocarcinoma via DNA damage.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2024
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4 more citing papers are in PubMed but not listed here.

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 4 institutions in 1 country.

Zhixian Wang *Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200071, P.R. China.
Xiao Zhang *Shanghai Institute of Thoracic Oncology, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai 200030, P.R. China.
Xiaoting TianShanghai Institute of Thoracic Oncology, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai 200030, P.R. China.
Yueyue YangDepartment of Clinical Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai 200072, P.R. China.
Lifang MaShanghai Institute of Thoracic Oncology, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai 200030, P.R. China.
Jiayi WangShanghai Institute of Thoracic Oncology, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai 200030, P.R. China.
Yongchun YuShanghai Institute of Thoracic Oncology, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai 200030, P.R. China.
Shanghai Chest Hospital · CNShanghai Jiao Tong University · CNShanghai University of Traditional Chinese Medicine · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis is a new form of regulated cell death and closely related to cancer. However, the mechanism underlying the regulation of ferroptosis in lung adenocarcinoma (LUAD) remains unclear. IB, IHC and ELISA were performed to analyze protein expression. RT‑qPCR was used to analyze mRNA expression. Cell viability, 3D cell growth, MDA, the generation of lipid ROS and the Fe2+ concentration were measured to evaluate the responses to the induction of ferroptosis. Measurement of luciferase activity and ChIP were used to analyze the promoter activity regulated by the transcriptional regulator. Co‑IP assays were performed to identify protein‑protein interactions. In the present study, it was revealed that cAMP response element‑binding protein (CREB) was highly expressed in LUAD, and knockdown of CREB inhibited cell viability and growth by promoting apoptosis‑ and ferroptosis‑like cell death, concurrently. It was observed that CREB suppressed lipid peroxidation by binding the promoter region of glutathione peroxidase 4 (GPX4), and this binding could be enhanced by E1A binding protein P300 (EP300). The bZIP domain in CREB and the CBP/p300‑HAT domain in EP300 were essential for CREB‑EP300 binding in LUAD cells. Finally, it was revealed that CREB, GPX4, EP300 and 4‑HNE were closely related to tumor size and stage, and tumors with a higher degree of malignancy were more likely to have a low degree of lipid peroxidation. Therefore, targeting this CREB/EP300/GPX4 axis may provide new strategies for treating LUAD.

Indexed as

Adenocarcinoma of LungCell Line, TumorCyclic AMP Response Element-Binding ProteinDatasets as TopicE1A-Associated p300 ProteinFerroptosisGene Expression Regulation, NeoplasticGene Knockdown TechniquesHEK293 CellsHumansLipid PeroxidationLungLung NeoplasmsPhospholipid Hydroperoxide Glutathione PeroxidasePromoter Regions, GeneticProtein BindingCREB1 protein, humanCyclic AMP Response Element-Binding ProteinE1A-Associated p300 ProteinEP300 protein, humanPhospholipid Hydroperoxide Glutathione Peroxidasecell deathE1A binding protein P300lipid peroxidationmethylationpromoter

Identifiers

PMID33846793
PMCPMC8042667
OpenAlexW3146768338

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.