Evidence map›Paper›PMID 27172794›Full record

ArticleOncotarget2016

EZH2 promotes colorectal cancer stem-like cell expansion by activating p21cip1-Wnt/β-catenin signaling.

Jian-Fang Chen, Xi Luo, Li-Sha Xiang, Hong-Tao Li, Lin Zha, Ni Li, Jian-Ming He, Gan-Feng Xie, Xiong Xie, Hou-Jie Liang

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

55 citing papers in PubMed, 73 citations in OpenAlex.

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  10. Mechanisms and Strategies to Overcome Drug Resistance in Colorectal Cancer.International journal of molecular sciences · 2025
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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 1 country.

Jian-Fang ChenDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China.
Xi LuoDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China.
Li-Sha XiangState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Sichuan, China.
Hong-Tao LiDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China.
Lin ZhaDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China.
Ni LiDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China.
Jian-Ming HeDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China.
Gan-Feng XieDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China.
Xiong XieDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China.
Hou-Jie LiangDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China.
Army Medical University · CNSouthwest Hospital · CNSichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Because colorectal cancer (CRC) stem-like cells (CCS-like cells) contribute to poor patient prognosis, these cells are a potential target for CRC therapy. However, the mechanism underlying the maintenance of CCS-like cell properties remains unclear. Here, we found that patients with advanced stage CRC expressed high levels of polycomb group protein enhancer of zeste homologue 2 (EZH2). High expression of EZH2 in tumor tissues correlated with poor patient prognosis. Conversely, silencing EZH2 reduced CRC cell proliferation. Surprisingly, EZH2 was more highly expressed in the CCS-like cell subpopulation than in the non-CCS-like cell subpopulation. EZH2 knockdown significantly reduced the CD133+/CD44+ subpopulation, suppressed mammosphere formation, and decreased the expression of self-renewal-related genes and strongly impaired tumor-initiating capacity in a re-implantation mouse model. Gene expression data from 433 human CRC specimens from TCGA database and in vitro results revealed that EZH2 helped maintain CCS-like cell properties by activating the Wnt/β-catenin pathway. We further revealed that p21cip1-mediated arrest of the cell cycle at G1/S phase is required for EZH2 activation of the Wnt/β-catenin pathway. Moreover, the specific EZH2 inhibitor EPZ-6438, a clinical trial drug, prevented CRC progression. Collectively, these findings revealed EZH2 maintaining CCS-like cell characteristics by arresting the cell cycle at the G1/S phase. These results indicate a new approach to CRC therapy.

Indexed as

Wnt Signaling PathwayAdultAgedAged, 80 and overAnimalsbeta CateninCell Line, TumorCell ProliferationColorectal NeoplasmsCyclin-Dependent Kinase Inhibitor p21Enhancer of Zeste Homolog 2 ProteinFemaleGene Expression Regulation, NeoplasticHumansMaleMicebeta CateninCDKN1A protein, humanCTNNB1 protein, humanCyclin-Dependent Kinase Inhibitor p21Enhancer of Zeste Homolog 2 ProteinEZH2 protein, humancancer stem-like cellcell cyclecolorectal cancerEZH2p21cip1

Identifiers

PMID27172794
PMCPMC5173077
OpenAlexW2346835588

What OpenQuestion holds

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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.