Evidence map›Paper›PMID 32382150›Full record

ArticleCell death & disease2020

LncRNA SNORD3A specifically sensitizes breast cancer cells to 5-FU by sponging miR-185-5p to enhance UMPS expression.

Liyun Luo, Jianlei Zhang, Hailin Tang, Dongfeng Zhai, Danqing Huang, Li Ling, Xiaorong Wang, Ting Liu, Qiong Zhang, Zhijie Zhang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
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  6. Identification of chromatin-associated RNAs at human centromeres.bioRxiv : the preprint server for biology · 2025
    Article
  7. Review
  8. Article
  9. SNORD3A Regulates STING Transcription to Promote Ferroptosis in Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  10. Review
  11. Review
  12. Article
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  16. Landscape of NcRNAs involved in drug resistance of breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  17. Review
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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

12 authors at 2 institutions in 1 country.

Liyun Luo *Affiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation; The State Key Laboratory of Respiratory; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment", Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Jianlei Zhang *Affiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation; The State Key Laboratory of Respiratory; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment", Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Hailin Tang *Department of Breast Oncology, State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Dongfeng Road 651 E, 510060, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0002-3206-782X
Dongfeng ZhaiAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation; The State Key Laboratory of Respiratory; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment", Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Danqing HuangAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation; The State Key Laboratory of Respiratory; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment", Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Li LingAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation; The State Key Laboratory of Respiratory; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment", Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Xiaorong WangAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation; The State Key Laboratory of Respiratory; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment", Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Ting LiuAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation; The State Key Laboratory of Respiratory; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment", Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Qiong ZhangAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation; The State Key Laboratory of Respiratory; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment", Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Zhijie ZhangAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation; The State Key Laboratory of Respiratory; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment", Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China. zjiezhang@126.com.
Zhimin HeAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation; The State Key Laboratory of Respiratory; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment", Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China. hezhimin2005@yahoo.com.
Guopei ZhengAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation; The State Key Laboratory of Respiratory; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment", Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China. zhengguopei@126.com.
Key Laboratory of Guangdong Province · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is the most common cancer type in women. Long non-coding RNAs (lncRNAs) have been reported as potential new diagnostic markers, prognostic factors, and therapeutic targets in cancer. However, the specific roles and mechanisms of lncRNAs in breast cancer remain to be elucidated. Here we demonstrated the downregulation of lncRNA SNORD3A in breast cancer cells and tissues and verified its non-protein-coding property. SNORD3A overexpression had no effect on cell proliferation but specifically sensitized breast cancer cells to 5-fluorouracil (5-FU) in vitro and in vivo. Mechanistically, SNORD3A exerts its effect via enhancing uridine monophosphate synthetase (UMPS) protein expression. SNORD3A acts as a competing endogenous RNA for miR-185-5p, leading to UMPS protein upregulation. miR-185-5p overexpression disrupted the effect of SNORD3A on chemosensitization to 5-FU in vitro and in vivo. Moreover, Meis1 overexpression transcriptionally promotes SNORD3A expression, and Meis1 is downregulated in breast cancer cells and tissues. In breast cancer tissues, SNORD3A level positively correlates with Meis1 and UMPS protein levels, whereas miR-185-5p level negatively correlates with UMPS protein level. High SNORD3A transcript and Meis1 and UMPS protein levels predicts a better outcome, but high miR-185-5p level predicts a worse outcome in breast cancer patients receiving 5-FU-based chemotherapy. Our findings indicate that Meis1-regulated SNORD3A specifically sensitizes breast cancer cells to 5-FU via enhancing UMPS expression. The SNORD3A-UMPS axis may serve as a potential biomarker and therapeutic target to improve the efficacy of 5-FU-based chemotherapy for breast cancer patients.

Indexed as

AnimalsBase SequenceBreast NeoplasmsCell Line, TumorDown-RegulationFemaleFluorouracilGene Expression Regulation, NeoplasticHumansMice, Inbred BALB CMice, NudeMicroRNAsMultienzyme ComplexesMyeloid Ecotropic Viral Integration Site 1 ProteinOrotate PhosphoribosyltransferaseOrotidine-5'-Phosphate DecarboxylaseFluorouracilMEIS1 protein, humanMicroRNAsMIRN185 microRNA, humanMultienzyme ComplexesMyeloid Ecotropic Viral Integration Site 1 ProteinOrotate PhosphoribosyltransferaseOrotidine-5'-Phosphate DecarboxylaseRNA, Long Noncodinguridine 5'-monophosphate synthase

Identifiers

PMID32382150
PMCPMC7205983
OpenAlexW3023388146

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Registered trials

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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.