Evidence map›Paper›PMID 31591481›Full record

ArticleOncogene2020

Oncogenic HOXB8 is driven by MYC-regulated super-enhancer and potentiates colorectal cancer invasiveness via BACH1.

Ying Ying, Yejun Wang, Xiaoyan Huang, Yanmei Sun, Junbao Zhang, Meiqi Li, Junhui Zeng, Maolin Wang, Wenjun Xiao, Lan Zhong and 5 more

Abstract read
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In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

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

  1. A Systematic Review onInternational journal of molecular sciences · 2021
    Pooled it
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  5. Acta pharmaceutica Sinica. B · 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

15 authors.

Ying Ying *Department of Physiology, School of Medicine, Health Science Center, Shenzhen University, 518060, Shenzhen, China.ORCID http://orcid.org/0000-0003-2128-3794
Yejun Wang *Department of Physiology, School of Medicine, Health Science Center, Shenzhen University, 518060, Shenzhen, China.
Xiaoyan HuangDepartment of Physiology, School of Medicine, Health Science Center, Shenzhen University, 518060, Shenzhen, China.
Yanmei SunDepartment of Physiology, School of Medicine, Health Science Center, Shenzhen University, 518060, Shenzhen, China.
Junbao ZhangDepartment of Physiology, School of Medicine, Health Science Center, Shenzhen University, 518060, Shenzhen, China.
Meiqi LiDepartment of Physiology, School of Medicine, Health Science Center, Shenzhen University, 518060, Shenzhen, China.
Junhui ZengDepartment of Physiology, School of Medicine, Health Science Center, Shenzhen University, 518060, Shenzhen, China.
Maolin WangDepartment of Physiology, School of Medicine, Health Science Center, Shenzhen University, 518060, Shenzhen, China.
Wenjun XiaoDepartment of Physiology, School of Medicine, Health Science Center, Shenzhen University, 518060, Shenzhen, China.
Lan ZhongDepartment of Gynecology and Obstetrics, West China Second Hospital, Sichuan University, 610041, Chengdu, China.
Bo XuTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, 300070, Tianjin, China.
Lili LiCancer Epigenetics Laboratory, Department of Clinical Oncology, Sir YK Pao Center for Cancer, The Chinese University of Hong Kong, 00000, Hong Kong, China.
Qian TaoCancer Epigenetics Laboratory, Department of Clinical Oncology, Sir YK Pao Center for Cancer, The Chinese University of Hong Kong, 00000, Hong Kong, China.
Xiaomei WangDepartment of Physiology, School of Medicine, Health Science Center, Shenzhen University, 518060, Shenzhen, China.
Xing-Sheng ShuDepartment of Physiology, School of Medicine, Health Science Center, Shenzhen University, 518060, Shenzhen, China. shu@szu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant activation of Homeobox genes in human cancers has long been documented, whereas the mechanisms underlying remain largely obscure. Super-enhancers (SEs) act as key regulatory elements for both cell identity genes and cancer genes. Herein, we reported that SE-associated HOXB gene cluster represented a common feature of colorectal cancer (CRC) cell lines and multiple HOXB genes within this cluster were overexpressed in CRC. Among them, we found that HOXB8 was oncogenic and its activation in CRC was driven by SE instead of genetic alteration. We further demonstrated that the master transcription factor MYC preferentially occupied SEs over TEs (typical enhancers) and regulated HOXB8 transcription by binding to the active elements of its SE. HOXB8 silencing induced reversal of transcriptional signatures associated with malignant phenotypes of CRC. Mechanistically, HOXB8 interacted with a key metastasis regulator BACH1 and instigated BACH1-mediated transcriptional cascade by directly occupying and activating BACH1 gene transcription together with BACH1 itself. Lastly, the relevance of HOXB8 activation in clinical settings was strengthened by its close association with prognostic outcomes of CRC patients.

Indexed as

CarcinogenesisAnimalsBasic-Leucine Zipper Transcription FactorsCell Line, TumorCell Transformation, NeoplasticColorectal NeoplasmsFemaleGene Expression Regulation, NeoplasticGene SilencingHomeodomain ProteinsHumansMaleMiceNeoplasm InvasivenessPhenotypeProto-Oncogene Proteins c-mycBACH1 protein, humanBasic-Leucine Zipper Transcription FactorsHomeodomain ProteinsHOXB8 protein, humanProto-Oncogene Proteins c-myc

Identifiers

What OpenQuestion holds

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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.