Evidence map›Paper›PMID 38049865›Full record

ArticleJournal of experimental & clinical cancer research : CR2023

SNORA56-mediated pseudouridylation of 28 S rRNA inhibits ferroptosis and promotes colorectal cancer proliferation by enhancing GCLC translation.

Chang Xu, Zhixuan Bian, Xinyue Wang, Na Niu, Li Liu, Yixuan Xiao, Jiabei Zhu, Nan Huang, Yue Zhang, Yan Chen and 4 more

Abstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

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

21 citing papers in PubMed.

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  14. Chemically modified non-coding RNAs in cancer.Expert reviews in molecular medicine · 2025
    Review
  15. Article
  16. Small nucleolar RNAs: the hidden precursors of cancer ribosomes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  17. Review
  18. Review
  19. Review
  20. SNORD3A Regulates STING Transcription to Promote Ferroptosis in Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
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

14 authors.

Chang Xu *Department of Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai, 200072, China.
Zhixuan Bian *Department of Laboratory Medicine, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
Xinyue Wang *Department of Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai, 200072, China.
Na NiuDepartment of Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai, 200072, China.
Li LiuDepartment of Laboratory Medicine, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
Yixuan XiaoDepartment of Laboratory Medicine, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
Jiabei ZhuDepartment of Laboratory Medicine, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
Nan HuangDepartment of Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai, 200072, China.
Yue ZhangDepartment of Central Laboratory, Shanghai Tenth People's Hospital of Tongji University, Shanghai, 200072, China.
Yan ChenDepartment of Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai, 200072, China.
Qi WuDepartment of Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai, 200072, China.
Fenyong SunDepartment of Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai, 200072, China.
Xiaoli ZhuDepartment of Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai, 200072, China. xiaolizhu@tongji.edu.cn.
Qiuhui PanDepartment of Laboratory Medicine, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China. panqiuhui@scmc.com.cn.

Funding

Science and Technology Innovation Plan Of Shanghai Science and Technology Commission 22JC1402300the Innovation Group Project of Shanghai Municipal Health Commission 2019CXJQ03the National Natural Science Foundation of China 81930066the National Natural Science Foundation of China 82172357the National Natural Science Foundation of China 82293662
6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) is one of the most common malignancies and is characterized by reprogrammed metabolism. Ferroptosis, a programmed cell death dependent on iron, has emerged as a promising strategy for CRC treatment. Although small nucleolar RNAs are extensively involved in carcinogenesis, it is unclear if they regulate ferroptosis during CRC pathogenesis.

methodsThe dysregulated snoRNAs were identified using published sequencing data of CRC tissues. The expression of the candidate snoRNAs, host gene and target gene were assessed by real-time quantitative PCR (RT-qPCR), fluorescence in situ hybridization (FISH), immunohistochemistry (IHC) and western blots. The biological function of critical molecules was investigated using in vitro and in vivo strategies including Cell Counting Kit-8 (CCK8), colony formation assay, flow cytometry, Fe

resultsHere, we investigated the SNORA56, which was elevated in CRC tissues and plasma, and correlated with CRC prognosis. SNORA56 deficiency in CRC impaired proliferation and triggered ferroptosis, resulting in reduced tumorigenesis. Mechanistically, SNORA56 mediated the pseudouridylation of 28 S rRNA at the U1664 site and promoted the translation of the catalytic subunit of glutamate cysteine ligase (GCLC), an indispensable rate-limiting enzyme in the biosynthesis of glutathione, which can inhibit ferroptosis by suppressing lipid peroxidation.

conclusionsTherefore, the SNORA56/28S rRNA/GCLC axis stimulates CRC progression by inhibiting the accumulation of cellular peroxides, and it may provide biomarker and therapeutic applications in CRC.

Indexed as

Colorectal NeoplasmsFerroptosisGlutamate-Cysteine LigaseRNA, Small NuclearAnimalsCarcinogenesisCell Line, TumorCell ProliferationHumansIn Situ Hybridization, FluorescenceMiceRNA, RibosomalGCLC protein, humanGlutamate-Cysteine LigaseRNA, RibosomalRNA, Small NuclearBiomarkerColorectal cancerFerroptosisGCLCProliferationPseudouridylationSNORA56Therapy

Identifiers

PMID38049865
PMCPMC10696674

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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.