Evidence map›Paper›PMID 27525719›Full record

ArticleNature cell biology2016

G9a/RelB regulates self-renewal and function of colon-cancer-initiating cells by silencing Let-7b and activating the K-RAS/β-catenin pathway.

Shih-Ting Cha, Ching-Ting Tan, Cheng-Chi Chang, Chia-Yu Chu, Wei-Jiunn Lee, Been-Zen Lin, Ming-Tsan Lin, Min-Liang Kuo

RetractedAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Nature cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. A biomechanical view of epigenetic tumor regulation.Journal of biological physics · 2023
    Review
  3. Matrine Protects Intestinal Barrier Function via MicroRNA-155 Through ROCK1-Signaling Pathway.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023
    Article
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  13. A link betweenOncotarget · 2017
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Shih-Ting ChaCenter for Systems Biology, National Taiwan University, Taipei 100, Taiwan.
Ching-Ting TanDepartment of Otolaryngology, National Taiwan University Hospital, Taipei 100, Taiwan.
Cheng-Chi ChangGraduate Institute of Oral Biology, School of Dentistry, National Taiwan University, Taipei 100, Taiwan.
Chia-Yu ChuDepartment of Dermatology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei 100, Taiwan.
Wei-Jiunn LeeDepartment of Urology, Wan Fang Hospital, Taipei Medical University, Taipei 110, Taiwan.
Been-Zen LinDepartment of Surgery, National Taiwan University Hospital, Taipei 100, Taiwan.
Ming-Tsan LinDepartment of Surgery, National Taiwan University Hospital, Taipei 100, Taiwan.
Min-Liang KuoInstitute of Biochemical Science, College of Life Science, National Taiwan University, Taipei 100, Taiwan.
National Taiwan University Hospital · TWKaohsiung Medical University · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic reprogramming has been associated with the functional plasticity of cancer-initiating cells (CICs); however, the regulatory pathway has yet to be elucidated. A siRNA screen targeting known epigenetic genes revealed that G9a profoundly impairs the chemo-resistance, self-renewal and metastasis of CICs obtained from patients with colorectal cancer (CRC). Patients with elevated G9a were shown to face a high risk of relapse and poor survival rates. From a mechanistic perspective, G9a binds with and stabilizes RelB, thereby recruiting DNA methyltransferase 3 on the Let-7b promoter and repressing its expression. This leads to the activation of the K-RAS/β-catenin pathway and regulates self-renewal and function of CICs. These findings indicate that the G9a/RelB/Let-7b axis acts as a critical regulator in the maintenance of CIC phenotypes and is strongly associated with negative clinical outcomes. Thus, these findings may have diagnostic as well as therapeutic implications for the treatment of chemotherapy-resistant or metastatic CRC.

Indexed as

Animalsbeta CateninColonColorectal NeoplasmsDrug Resistance, NeoplasmGene SilencingGenes, rasHistocompatibility AntigensHistone-Lysine N-MethyltransferaseHumansMiceMicroRNAsNeoplastic Stem CellsPhenotypeTranscription Factor RelBWnt Signaling Pathwaybeta CateninEHMT2 protein, humanG9a protein, mouseHistocompatibility AntigensHistone-Lysine N-MethyltransferaseMicroRNAsmirnlet7 microRNA, humanmirnlet7 microRNA, mouseRELB protein, humanRelb protein, mouseTranscription Factor RelB

Identifiers

PMID27525719
OpenAlexW2510794305

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.