Evidence map›Paper›PMID 34609966›Full record

ArticleThe Journal of clinical investigation2021

RBMS1 regulates lung cancer ferroptosis through translational control of SLC7A11.

Wenjing Zhang, Yu Sun, Lu Bai, Lili Zhi, Yun Yang, Qingzhi Zhao, Chaoqun Chen, Yangfan Qi, Wenting Gao, Wenxia He and 16 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 183 papers.

0numbers the graph read from it
0cells of the map it votes in
183citing papers in PubMed
28.8field-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

183 citing papers in PubMed, 273 citations in OpenAlex.

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  11. PSMA8-Containing 20S Proteasome Regulates Spermiogenesis and Male Fertility.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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123 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

26 authors at 6 institutions in 2 countries.

Wenjing ZhangInstitute of Cancer Stem Cells and Second Affiliated Hospital, Dalian Medical University, Dalian, China.
Yu SunInstitute of Cancer Stem Cells and Second Affiliated Hospital, Dalian Medical University, Dalian, China.
Lu BaiInstitute of Cancer Stem Cells and Second Affiliated Hospital, Dalian Medical University, Dalian, China.
Lili ZhiInstitute of Cancer Stem Cells and Second Affiliated Hospital, Dalian Medical University, Dalian, China.
Yun YangCAS-MPG Partner Institute for Computational Biology, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, Shanghai, China.
Qingzhi ZhaoInstitute of Cancer Stem Cells and Second Affiliated Hospital, Dalian Medical University, Dalian, China.
Chaoqun ChenInstitute of Cancer Stem Cells and Second Affiliated Hospital, Dalian Medical University, Dalian, China.
Yangfan QiInstitute of Cancer Stem Cells and Second Affiliated Hospital, Dalian Medical University, Dalian, China.
Wenting GaoInstitute of Genome Engineered Animal Models for Human Diseases.
Wenxia HeInstitute of Cancer Stem Cells and Second Affiliated Hospital, Dalian Medical University, Dalian, China.
Luning WangInstitute of Cancer Stem Cells and Second Affiliated Hospital, Dalian Medical University, Dalian, China.
Dan ChenDepartment of Pathology, First Affiliated Hospital, and.
Shujun FanDepartment of Pathology, Dalian Medical University, Dalian, China.
Huan ChenCAS Key Laboratory of Separation Science for Analytical Chemistry, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China.
Hai-Long PiaoCAS Key Laboratory of Separation Science for Analytical Chemistry, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China.
Qinglong QiaoCAS Key Laboratory of Separation Science for Analytical Chemistry, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China.
Zhaochao XuCAS Key Laboratory of Separation Science for Analytical Chemistry, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China.
Jinrui ZhangInstitute of Cancer Stem Cells and Second Affiliated Hospital, Dalian Medical University, Dalian, China.
Jinyao ZhaoInstitute of Cancer Stem Cells and Second Affiliated Hospital, Dalian Medical University, Dalian, China.
Sirui ZhangCAS-MPG Partner Institute for Computational Biology, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, Shanghai, China.
Yue YinNational Facility for Protein Science in Shanghai, Zhangjiang Lab, Shanghai Advanced Research Institute, Chinese Academy of Science, Shanghai, China.
Chao PengNational Facility for Protein Science in Shanghai, Zhangjiang Lab, Shanghai Advanced Research Institute, Chinese Academy of Science, Shanghai, China.
Xiaoling LiSignal Transduction Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Quentin LiuInstitute of Cancer Stem Cells and Second Affiliated Hospital, Dalian Medical University, Dalian, China.
Han LiuInstitute of Cancer Stem Cells and Second Affiliated Hospital, Dalian Medical University, Dalian, China.
Yang WangInstitute of Cancer Stem Cells and Second Affiliated Hospital, Dalian Medical University, Dalian, China.
Dalian Medical University · CNDalian Institute of Chemical Physics · CNShanghai Advanced Research Institute · CNShanghai Institute of Nutrition and Health · CNHuman Genome Sciences (United States) · USNational Institute of Environmental Health Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis, an iron-dependent nonapoptotic cell death, is a highly regulated tumor suppressing process. However, functions and mechanisms of RNA-binding proteins in regulation of evasion of ferroptosis during lung cancer progression are still largely unknown. Here, we report that the RNA-binding protein RBMS1 participates in lung cancer development via mediating ferroptosis evasion. Through an shRNA-mediated systematic screen, we discovered that RBMS1 is a key ferroptosis regulator. Clinically, RBMS1 was elevated in lung cancer and its high expression was associated with reduced patient survival. Conversely, depletion of RBMS1 inhibited lung cancer progression both in vivo and in vitro. Mechanistically, RBMS1 interacted with the translation initiation factor eIF3d directly to bridge the 3'- and 5'-UTR of SLC7A11. RBMS1 ablation inhibited the translation of SLC7A11, reduced SLC7A11-mediated cystine uptake, and promoted ferroptosis. In a drug screen that targeted RBMS1, we further uncovered that nortriptyline hydrochloride decreased the level of RBMS1, thereby promoting ferroptosis. Importantly, RBMS1 depletion or inhibition by nortriptyline hydrochloride sensitized radioresistant lung cancer cells to radiotherapy. Our findings established RBMS1 as a translational regulator of ferroptosis and a prognostic factor with therapeutic potential and clinical value.

Indexed as

Protein BiosynthesisAmino Acid Transport System y+AnimalsCell Line, TumorDNA-Binding ProteinsFerroptosisHEK293 CellsHumansLung NeoplasmsMiceProto-Oncogene Proteins c-etsRadiation ToleranceRNA-Binding ProteinsTranscription FactorsAmino Acid Transport System y+DNA-Binding ProteinsELF3 protein, humanProto-Oncogene Proteins c-etsRBMS1 protein, humanRNA-Binding ProteinsSLC7A11 protein, humanTranscription FactorsCell BiologyLung cancerMolecular biologyOncologyTranslation

Identifiers

PMID34609966
PMCPMC8592553
OpenAlexW3203095800

What OpenQuestion holds

Textmetadata
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.