Evidence map›Paper›PMID 30696957›Full record

ArticleOncogene2019

Lymphoid enhancer-binding factor-1 promotes stemness and poor differentiation of hepatocellular carcinoma by directly activating the NOTCH pathway.

Shuo Fang, Ming Liu, Lei Li, Fei-Fei Zhang, Yun Li, Qian Yan, Yu-Zhu Cui, Ying-Hui Zhu, Yun-Fei Yuan, Xin-Yuan Guan

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

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

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Role of Notch signaling pathway in joint homeostasis and osteoarthritis.Frontiers in bioengineering and biotechnology · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Hepatocellular carcinoma: signaling pathways and therapeutic advances.Signal transduction and targeted therapy · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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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

10 authors at 3 institutions in 2 countries.

Shuo FangDepartment of Clinical Oncology, The University of Hong Kong, Hong Kong, China.
Ming LiuKey Laboratory of Protein Modification and Degradation School of Basic Medical Sciences, Guangzhou Medical University, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, China.
Lei LiState Key Laboratory of Oncology in Southern China, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Fei-Fei ZhangDepartment of Clinical Oncology, The University of Hong Kong, Hong Kong, China.
Yun LiDepartment of Clinical Oncology, The University of Hong Kong, Hong Kong, China.
Qian YanDepartment of Clinical Oncology, The University of Hong Kong, Hong Kong, China.
Yu-Zhu CuiDepartment of Clinical Oncology, The University of Hong Kong, Hong Kong, China.
Ying-Hui ZhuState Key Laboratory of Oncology in Southern China, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Yun-Fei YuanState Key Laboratory of Oncology in Southern China, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Xin-Yuan GuanDepartment of Clinical Oncology, The University of Hong Kong, Hong Kong, China. xyguan@hku.hk.ORCID http://orcid.org/0000-0002-4485-6017
Sun Yat-sen University · CNChinese University of Hong Kong · HKGuangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The poorly differentiated hepatocellular carcinoma (HCC) cells are usually characterized by immature hepatic progenitor cell-like properties, such as enhanced self-renewal ability, resistance to chemotherapeutic drugs, and a loss of mature hepatocyte proteins. However, the molecular mechanisms governing this process still remain unclear. In this study, we found the lymphoid enhancer-binding factor-1 (LEF1), a transcriptional factor, was frequently overexpressed in HCCs, which was significantly associated with poor prognosis and tumor cell differentiation. Functional studies have found that LEF1 enhanced cell growth, foci formation, colony formation in soft agar, and tumor formation in nude mice. Different from its canonical roles in the WNT signaling pathway, we found that LEF1 could activate the critical members (e.g., NOTCH1 and NOTCH2) of the NOTCH signaling pathway through directly binding to their promoter regions. Further studies have found that LEF1 could enhance the self-renewal ability, drug resistance, dedifferentiation, and invasion of HCC cells. The oncogenic functions and the effects of LEF1 on cancer stemness could be effectively inhibited by NOTCH inhibitor. Further characterization of LEF1 may lead to the development of novel therapeutic strategies for HCC treatment.

Indexed as

AnimalsCarcinogenesisCarcinoma, HepatocellularCell DifferentiationCell Line, TumorCell ProliferationHep G2 CellsHumansLiver NeoplasmsLymphoid Enhancer-Binding Factor 1MiceMice, NudePrognosisPromoter Regions, GeneticReceptors, NotchTranscription FactorsLEF1 protein, humanLymphoid Enhancer-Binding Factor 1Receptors, NotchTranscription Factors

Identifiers

PMID30696957
OpenAlexW2911325539

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.