Evidence map›Paper›PMID 33767438›Full record

ArticleOncogene2021

BCL9/BCL9L promotes tumorigenicity through immune-dependent and independent mechanisms in triple negative breast cancer.

Xiaoshuang Wang, Mei Feng, Tengfei Xiao, Baosen Guo, Danyang Liu, Chenglong Liu, Jinpeng Pei, Qiaofeng Liu, Yi Xiao, Rina Rosin-Arbesfeld and 8 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Targeting BCL9/BCL9L enhances CD4Acta pharmacologica Sinica · 2026
    Article
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  15. Potential role of PIM1 inhibition in the treatment of SARS-CoV-2 infection.Journal, genetic engineering & biotechnology · 2023
    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

18 authors at 5 institutions in 2 countries.

Xiaoshuang Wang *Department of Pharmacology, School of Pharmacy, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-0725-9440
Mei Feng *Department of Pharmacology, School of Pharmacy, Fudan University, Shanghai, China.
Tengfei XiaoXBH Biotech, Shanghai, China.
Baosen GuoShenzhen Digital Life Institute, Shenzhen, Guangdong, China.ORCID http://orcid.org/0000-0001-7554-8677
Danyang LiuObstetrics & Gynecology Hospital of Fudan University, Shanghai, China.
Chenglong LiuDepartment of Pharmacology, School of Pharmacy, Fudan University, Shanghai, China.
Jinpeng PeiDepartment of Pharmacology, School of Pharmacy, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-3467-5458
Qiaofeng LiuDepartment of Pharmacology, School of Pharmacy, Fudan University, Shanghai, China.
Yi XiaoDepartment of Surgery in Breast Cancer, Fudan University Shanghai Cancer Center, Shanghai, China.
Rina Rosin-ArbesfeldDepartment of Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Ying ShiDepartment of Pharmacology, School of Pharmacy, Fudan University, Shanghai, China.
Yang ZhouDepartment of Pharmacology, School of Pharmacy, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-7213-2518
Mengxuan YangThe First Affiliated Hospital, Zhejiang University School of Medicine, Institute of Translational Medicine, Zhejiang University, Hangzhou, China.
Yu-Xiong FengThe First Affiliated Hospital, Zhejiang University School of Medicine, Institute of Translational Medicine, Zhejiang University, Hangzhou, China.
Yizhou JiangDepartment of Surgery in Breast Cancer, Fudan University Shanghai Cancer Center, Shanghai, China.ORCID http://orcid.org/0000-0003-3699-2630
Zhimin ShaoDepartment of Surgery in Breast Cancer, Fudan University Shanghai Cancer Center, Shanghai, China.
Ker YuDepartment of Pharmacology, School of Pharmacy, Fudan University, Shanghai, China. keryu@fudan.edu.cn.ORCID http://orcid.org/0000-0002-0607-0531
Di ZhuDepartment of Pharmacology, School of Pharmacy, Fudan University, Shanghai, China. zhudi@fudan.edu.cn.ORCID http://orcid.org/0000-0003-4622-4600
Fudan University · CNFudan University Shanghai Cancer Center · CNFirst Affiliated Hospital Zhejiang University · CNObstetrics and Gynecology Hospital of Fudan University · CNTel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Treatment of patients with triple-negative breast cancer (TNBC) has been challenging due to a lack of well-defined molecular targets. The Wnt/β-catenin pathway is known to be activated in many TNBC patients and BCL9 and BCL9L are important transcriptional co-activators of β-catenin, but whether inhibition of BCL9/BCL9L can suppress TNBC growth and the underlying mechanism are not fully understood. Here we demonstrate that the expression of BCL9 and BCL9L is directly correlated with malignancy in TNBC patient tumors and that BCL9 and BCL9L promote tumor cell growth, cell migration and metastasis in TNBC models. Mechanistically, we found that BCL9/BCL9L promotes tumorigenicity through both the Wnt and TGF-β pathways. Besides, BCL9/BCL9L expression inversely correlates with CD8

Indexed as

AnimalsCD8-Positive T-LymphocytesCell ProliferationDNA-Binding ProteinsHumansMCF-7 CellsMiceMice, NudeTranscription FactorsTriple Negative Breast NeoplasmsTumor MicroenvironmentBCL9L protein, humanBCL9L protein, mouseBCL9 protein, humanBCL9 protein, mouseDNA-Binding ProteinsTranscription Factors

Identifiers

PMID33767438
OpenAlexW3138793175

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.