Evidence map›Paper›PMID 35461328›Full record

ArticleOncogene2022

MUC1 triggers lineage plasticity of Her2 positive mammary tumors.

Zhi Pang, Xinran Dong, Huayun Deng, Chengzhi Wang, Xiaodong Liao, Chunhua Liao, Yahui Liao, Weidong Tian, Jinke Cheng, Guoqiang Chen and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

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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

12 authors at 3 institutions in 2 countries.

Zhi Pang *Department of Histoembryology, Genetics and Developmental Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory of Reproductive Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.ORCID http://orcid.org/0000-0001-8677-9008
Xinran Dong *Center for Molecular Medicine, Children's Hospital of Fudan University, Shanghai, People's Republic of China.ORCID http://orcid.org/0000-0001-9868-8795
Huayun Deng *Department of Histoembryology, Genetics and Developmental Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory of Reproductive Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.ORCID http://orcid.org/0000-0002-5909-625X
Chengzhi WangDepartment of Histoembryology, Genetics and Developmental Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory of Reproductive Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.ORCID http://orcid.org/0000-0003-2303-5559
Xiaodong LiaoDepartment of Histoembryology, Genetics and Developmental Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory of Reproductive Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.ORCID http://orcid.org/0000-0001-9230-5220
Chunhua LiaoDepartment of Histoembryology, Genetics and Developmental Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory of Reproductive Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.ORCID http://orcid.org/0000-0002-4868-0936
Yahui LiaoDepartment of Pharmacy, Huangpu branch of the Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.ORCID http://orcid.org/0000-0003-4610-9071
Weidong TianCenter for Molecular Medicine, Children's Hospital of Fudan University, Shanghai, People's Republic of China.
Jinke ChengDepartment of Histoembryology, Genetics and Developmental Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory of Reproductive Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.ORCID http://orcid.org/0000-0002-4344-5363
Guoqiang ChenDepartment of Histoembryology, Genetics and Developmental Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory of Reproductive Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.ORCID http://orcid.org/0000-0003-4936-2363
Haiying YiDepartment of Breast Surgery, Huangpu branch of the Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China. yihaiying@163.com.ORCID http://orcid.org/0000-0001-7439-3968
Lei HuangDepartment of Histoembryology, Genetics and Developmental Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory of Reproductive Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China. leihuang@shsmu.edu.cn.ORCID http://orcid.org/0000-0002-4851-4807
Shanghai Jiao Tong University · CNChildren's Hospital of Fudan University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant overexpression of mucin 1 (MUC1) and human epidermal growth factor receptor 2 (HER2) are often observed in breast cancer. However, the role of concomitant MUC1/HER2 in the development of breast cancer has not been fully illustrated. Following analysis of public microarray datasets that revealed a correlation between double MUC1 and HER2 positivity and a worse clinical outcome, we generated a mouse model overexpressing both Her2 and MUC1 cytoplasmic domain (MUC1-CD) to investigate their interaction in mammary carcinogenesis. Coexpression of Her2 and MUC1-CD conferred a growth advantage and promoted the development of spontaneous mammary tumors. Genomic analysis revealed that enforced expression of MUC1-CD and Her2 induces mammary tumor lineage plasticity, which is supported by gene reprogramming and mammary stem cell enrichment. Through gain- and loss-of-function strategies, we show that coexpression of Her2 and MUC1-CD is associated with downregulation of tricarboxylic acid (TCA) cycle genes in tumors. Importantly, the reduction in TCA cycle genes induced by MUC1-CD was found to be significantly connected to poor prognosis in HER2

Indexed as

Breast NeoplasmsMammary Neoplasms, AnimalAnimalsCell Transformation, NeoplasticErb-b2 Receptor Tyrosine KinasesFemaleHumansMiceMucin-1Signal TransductionErb-b2 Receptor Tyrosine KinasesMUC1 protein, humanmuc1 protein, mouseMucin-1

Identifiers

PMID35461328
OpenAlexW4224233746

What Socratic 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 Socratic graph.