Evidence map›Paper›PMID 37248295›Full record

ArticleCommunications biology2023

KLF11 regulates lung adenocarcinoma ferroptosis and chemosensitivity by suppressing GPX4.

Guangyin Zhao, Jiaqi Liang, Guangyao Shan, Jie Gu, Fengkai Xu, Chunlai Lu, Teng Ma, Guoshu Bi, Cheng Zhan, Di Ge

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

Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.2field-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

24 citing papers in PubMed, 34 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

10 authors at 1 institution in 1 country.

Guangyin Zhao *Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Jiaqi Liang *Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Guangyao Shan *Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Jie GuDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Fengkai XuDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Chunlai LuDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Teng MaDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Guoshu BiDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Cheng ZhanDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China. czhan10@fudan.edu.cn.ORCID 0000-0001-8745-9276
Di GeDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China. ge.di@zs-hospital.sh.cn.ORCID 0000-0001-5241-1766
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis, an iron-dependent non-apoptotic cell death, has been shown to play a vital role in tumor proliferation and chemotherapy resistance. Here, we report that KLF11 inhibits lung adenocarcinoma (LUAD) cell proliferation and promotes chemotherapy sensitivity by participating in the GPX4-related ferroptosis pathway. Through an RNA-sequence screen from LUAD cells pretreatment with ferroptosis inducers (FINs), we discovered that KLF11 expression was significantly higher in FINs-treated cells, suggesting that KLF11 may be involved in ferroptosis. Overexpression of KLF11 promoted LUAD cells to undergo ferroptosis alterations. Meanwhile, upregulation of KLF11 expression also inhibited cell proliferation and increased chemosensitivity, whereas knockout of KLF11 did the opposite. With ChIP-Seq and RNA-Seq, we identified GPX4 as a downstream target of KLF11. Through ChIP-qPCR and dual luciferase assay, we clarified that KLF11 binds to the promoter region of GPX4 and represses its transcription. Restored GPX4 expression antagonized the ability of KLF11 to promote ferroptosis, increase chemotherapy sensitivity and inhibit cell proliferation in vitro and in vivo. Clinically, KLF11 declined in LUAD and its low expression was associated with reduced patient survival. Our findings established the function of KLF11 to promote ferroptosis in LUAD, thereby inhibiting cell proliferation and enhancing the efficacy of chemotherapy.

Indexed as

Adenocarcinoma of LungApoptosis Regulatory ProteinsFerroptosisPhospholipid Hydroperoxide Glutathione PeroxidaseRepressor ProteinsCell Line, TumorCell ProliferationHumansMitochondriaApoptosis Regulatory ProteinsGPX4 protein, humanKLF11 protein, humanPhospholipid Hydroperoxide Glutathione PeroxidaseRepressor Proteins

Identifiers

PMID37248295
PMCPMC10227016
OpenAlexW4378717214

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.