Evidence map›Paper›PMID 38520019›Full record

ArticleMolecular cancer2024

LINC00115 promotes chemoresistant breast cancer stem-like cell stemness and metastasis through SETDB1/PLK3/HIF1α signaling.

Fei Luo, Mingda Zhang, Bowen Sun, Chenxin Xu, Yi Yang, Yingwen Zhang, Shanshan Li, Guoyu Chen, Ceshi Chen, Yanxin Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
10.8field-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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
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  11. Review
  12. The Many Faces of SetDB1.Epigenomes · 2026
    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

11 authors at 4 institutions in 1 country.

Fei Luo *State Key Laboratory of Systems Medicine for Cancer, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Mingda Zhang *State Key Laboratory of Systems Medicine for Cancer, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Bowen Sun *State Key Laboratory of Systems Medicine for Cancer, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Chenxin XuState Key Laboratory of Systems Medicine for Cancer, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Yi YangPediatric Translational Medicine Institute, Department of Hematology & Oncology, Committee Key Laboratory of Pediatric Hematology & Oncology, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, National Health Committee Key Laboratory of Pediatric Hematology & Oncology, Shanghai, 200127, China.
Yingwen ZhangState Key Laboratory of Systems Medicine for Cancer, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Shanshan LiPediatric Translational Medicine Institute, Department of Hematology & Oncology, Committee Key Laboratory of Pediatric Hematology & Oncology, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, National Health Committee Key Laboratory of Pediatric Hematology & Oncology, Shanghai, 200127, China.
Guoyu ChenState Key Laboratory of Systems Medicine for Cancer, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Ceshi ChenAcademy of Biomedical Engineering, the Third Affiliated Hospital, Kunming Medical University, Kunming, 650500, China. chenc@kmmu.edu.cn.
Yanxin LiPediatric Translational Medicine Institute, Department of Hematology & Oncology, Committee Key Laboratory of Pediatric Hematology & Oncology, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, National Health Committee Key Laboratory of Pediatric Hematology & Oncology, Shanghai, 200127, China. liyanxincau@163.com.
Haizhong FengState Key Laboratory of Systems Medicine for Cancer, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China. fenghaizhong@sjtu.edu.cn.
Shanghai Cancer Institute · CNShanghai Jiao Tong University · CNShanghai Children's Medical Center · CNKunming Medical University · CN

Funding

National Key Research and Development Program of China 2022YFA1104001National Natural Science Foundation of China 32371004, 82103657, 82072896, and 81972341the Program of Shanghai Academic/Technology Research Leader 21XD1403100the Shanghai Municipal Science and Technology Commission 21ZR1439500
6 · The paper itself

Abstract

backgroundCancer stem-like cell is a key barrier for therapeutic resistance and metastasis in various cancers, including breast cancer, yet the underlying mechanisms are still elusive. Through a genome-wide lncRNA expression profiling, we identified that LINC00115 is robustly upregulated in chemoresistant breast cancer stem-like cells (BCSCs).

methodsLncRNA microarray assay was performed to document abundance changes of lncRNAs in paclitaxel (PTX)-resistant MDA-MB-231 BCSC (ALDH

resultsLINC00115 functions as a scaffold lncRNA to link SETDB1 and PLK3, leading to enhanced SETDB1 methylation of PLK3 at both K106 and K200 in drug-resistant BCSC. PLK3 methylation decreases PLK3 phosphorylation of HIF1α and thereby increases HIF1α stability. HIF1α, in turn, upregulates ALKBH5 to reduce m

conclusionsOur findings uncover LINC00115 as a critical regulator of BCSC and highlight targeting LINC00115 and SETDB1 as a potential therapeutic strategy for chemotherapeutic resistant breast cancer.

Indexed as

RNA, Long NoncodingTriple Negative Breast NeoplasmsAnimalsBreastCell Line, TumorDisease Models, AnimalHistone-Lysine N-MethyltransferaseHumansNeoplastic Stem CellsPaclitaxelPolo-like KinasesProtein Serine-Threonine KinasesSignal TransductionTumor Suppressor ProteinsHistone-Lysine N-MethyltransferasePaclitaxelPLK3 protein, humanPolo-like KinasesProtein Serine-Threonine KinasesRNA, Long NoncodingSETDB1 protein, humanTumor Suppressor ProteinsCancer stem-like cellsHIF1αLINC00115Lysine methylationTherapeutic resistanceTriple-negative breast cancer

Identifiers

PMID38520019
PMCPMC10958889
OpenAlexW4393077536

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.