Evidence map›Paper›PMID 30002443›Full record

ArticleOncogene2018

LINC01638 lncRNA activates MTDH-Twist1 signaling by preventing SPOP-mediated c-Myc degradation in triple-negative breast cancer.

Liyun Luo, Hailin Tang, Li Ling, Nan Li, Xiaoting Jia, Zhijie Zhang, Xiaorong Wang, Lejuan Shi, Jiang Yin, Ni Qiu and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 1 pooled it
12.5field-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

82 citing papers in PubMed, 1 synthesis or guideline pooled it, 149 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Molecular insights for the tumor suppressor role of SPOP in prostate cancer.Biochimica et biophysica acta. Reviews on cancer · 2026
    Review
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  19. LncRNA BCAN-AS1 stabilizes c-Myc via NCell death and differentiation · 2023
    Article
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22 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

17 authors at 2 institutions in 1 country.

Liyun LuoAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment"; Protein Modification and Degradation Lab, Guangzhou Medical University, Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Hailin TangDepartment 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.
Li LingAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment"; Protein Modification and Degradation Lab, Guangzhou Medical University, Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Nan LiAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment"; Protein Modification and Degradation Lab, Guangzhou Medical University, Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Xiaoting JiaAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment"; Protein Modification and Degradation Lab, Guangzhou Medical University, Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Zhijie ZhangAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment"; Protein Modification and Degradation Lab, Guangzhou Medical University, Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Xiaorong WangAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment"; Protein Modification and Degradation Lab, Guangzhou Medical University, Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Lejuan ShiAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment"; Protein Modification and Degradation Lab, Guangzhou Medical University, Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Jiang YinAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment"; Protein Modification and Degradation Lab, Guangzhou Medical University, Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Ni QiuAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment"; Protein Modification and Degradation Lab, Guangzhou Medical University, Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Hao LiuAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment"; Protein Modification and Degradation Lab, Guangzhou Medical University, Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Ying SongAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment"; Protein Modification and Degradation Lab, Guangzhou Medical University, Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Kai LuoAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment"; Protein Modification and Degradation Lab, Guangzhou Medical University, Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Hongsheng LiAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment"; Protein Modification and Degradation Lab, Guangzhou Medical University, Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Zhimin HeAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment"; Protein Modification and Degradation Lab, Guangzhou Medical University, Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.
Guopei ZhengAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment"; Protein Modification and Degradation Lab, Guangzhou Medical University, Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China. zhengguopei@126.com.
Xiaoming XieDepartment 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. xiexm@sysucc.org.cn.
Guangzhou Medical University · CNSun Yat-sen University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81401989National Natural Science Foundation of China (National Science Foundation of China) 81672616National Natural Science Foundation of China (National Science Foundation of China) 81772961
6 · The paper itself

Abstract

Breast cancer is a heterogeneous disease, and triple-negative breast cancer (TNBC) continues to be a serious health problem. The potential involvement of lncRNAs in TNBC progression remains unexplored. Here, we demonstrated that LINC01638 is highly expressed in TNBC tissues and cells. LINC01638 maintains the mesenchymal traits of TNBC cells, including an enriched epithelial-mesenchymal transition (EMT) signature and cancer stem cell-like state. LINC01638 knockdown suppresses tumor proliferation and metastasis both in vitro and in vivo. LINC01638 overexpression predicts a poor outcome of breast cancer patients. Mechanistically, LINC01638 interacts with c-Myc to prevent SPOP-mediated c-Myc ubiquitination and degradation. C-Myc transcriptionally enhances MTDH (metadherin) expression and subsequently activates Twist1 expression to induce EMT. Our findings describe LINC01638-mediated signal transduction and highlight the crucial role of LINC01638 in TNBC progression.

Indexed as

AnimalsCell Adhesion MoleculesCell Line, TumorCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHeterograftsHumansMCF-7 CellsMembrane ProteinsMiceMice, Inbred BALB CNeoplastic Stem CellsNuclear ProteinsPhenotypeCell Adhesion MoleculesMembrane ProteinsMTDH protein, humanMYC protein, humanNuclear ProteinsProto-Oncogene Proteins c-mycRepressor ProteinsRNA-Binding ProteinsRNA, Long NoncodingSPOP protein, humanTranscription FactorsTWIST1 protein, humanTwist-Related Protein 1

Identifiers

PMID30002443
OpenAlexW2835650704

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.