Evidence map›Paper›PMID 28796259›Full record

ArticleCell death & disease2017

MUC1 induces acquired chemoresistance by upregulating ABCB1 in EGFR-dependent manner.

Wei Jin, Xiaodong Liao, Yaping Lv, Zhi Pang, Yuming Wang, Quanfu Li, Yahui Liao, Qing Ye, Guoqiang Chen, Kewen Zhao and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
2.5field-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

64 citing papers in PubMed, 92 citations in OpenAlex.

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4 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 1 country.

Wei JinKey Laboratory of Cell Differentiation and Apoptosis of The Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaodong LiaoKey Laboratory of Cell Differentiation and Apoptosis of The Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yaping LvKey Laboratory of Cell Differentiation and Apoptosis of The Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zhi PangKey Laboratory of Cell Differentiation and Apoptosis of The Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yuming WangDepartment of Cardiothoracic Surgery, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Quanfu LiKey Laboratory of Cell Differentiation and Apoptosis of The Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yahui LiaoKey Laboratory of Cell Differentiation and Apoptosis of The Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Qing YeDepartment of Cardiothoracic Surgery, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Guoqiang ChenKey Laboratory of Cell Differentiation and Apoptosis of The Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Kewen ZhaoKey Laboratory of Cell Differentiation and Apoptosis of The Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Lei HuangKey Laboratory of Cell Differentiation and Apoptosis of The Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shanghai Jiao Tong University · CNRenji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemoresistance contributes to cancer relapse and increased mortality in a variety of cancer types, raising a pressing need to better understand the underlying mechanism. MUC1 is abnormally overexpressed in numerous carcinomas and associated with poor prognosis. However, the functional significance of MUC1 in chemoresistance has not been fully elucidated. Here, we showed that MUC1 expression was considerably induced in cells that had acquired chemoresistance at both transcriptional and post-translational levels. Using gain- and loss-of function approaches, we demonstrated a critical role of MUC1 in induction of drug resistance. Through stimulation of EGFR activation and nuclear translocation, MUC1 increased the expression of ATP-binding cassette transporter B1 (ABCB1). Remarkably, targeted suppression of EGFR or ABCB1 by both shRNAs and inhibitors effectively reversed chemoresistance. Moreover, co-administration of the inhibitors of MUC1-EGFR-ABCB1 with paclitaxel significantly blocked not only tumor growth but also relapse in xenograft mouse model. Our data collectively support a model in which MUC1 induces acquired chemotherapy resistance by upregulating ABCB1 in an EGFR-dependent manner, providing a novel molecular basis of using the EGFR inhibitor in MUC1-positive cancers to prevent chemotherapy resistance.

Indexed as

AnimalsAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily B, Member 1Blotting, WesternCell Line, TumorCell ProliferationCell SurvivalChromatin ImmunoprecipitationErbB ReceptorsErlotinib HydrochlorideFemaleFluorescent Antibody TechniqueGene Expression Regulation, NeoplasticHEK293 CellsHumansImmunoprecipitationAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily B, Member 1ErbB ReceptorsErlotinib HydrochlorideMucin-1

Identifiers

PMID28796259
PMCPMC5596566
OpenAlexW2743713824

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.