Evidence map›Paper›PMID 29181633›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2018

Amphiregulin regulates proliferation and migration of HER2-positive breast cancer cells.

Hannah Schmucker, Walker M Blanding, Julia M Mook, Jessica F Wade, Jang Pyo Park, Kerri Kwist, Hiral Shah, Brian W Booth

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

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  9. ILC2s: New Actors in Tumor Immunity.Frontiers in immunology · 2019
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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

8 authors at 1 institution in 1 country.

Hannah SchmuckerDepartment of Biological Sciences, Clemson University, Clemson, SC, USA.
Walker M BlandingDepartment of Biological Sciences, Clemson University, Clemson, SC, USA.
Julia M MookDepartment of Microbiology, Clemson University, Clemson, SC, USA.
Jessica F WadeDepartment of Biological Sciences, Clemson University, Clemson, SC, USA.
Jang Pyo ParkInstitute for Biological Interfaces of Engineering, Clemson University, Clemson, SC, USA.
Kerri KwistInstitute for Biological Interfaces of Engineering, Clemson University, Clemson, SC, USA.
Hiral ShahDepartment of Bioengineering, Institute for Biological Interfaces of Engineering, Clemson University, 401-1 Rhodes Engineering Research Center, Clemson, SC, 29634, USA.
Brian W BoothInstitute for Biological Interfaces of Engineering, Clemson University, Clemson, SC, USA. brbooth@clemson.edu.ORCID http://orcid.org/0000-0003-2542-7302
Clemson University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTumor initiation and progression rely on cellular proliferation and migration. Many factors are involved in these processes, including growth factors. Amphiregulin (AREG) is involved in normal mammary development and the development of estrogen receptor (ER)-positive breast cancer. The aim of this project was to determine if AREG is involved in the proliferation and progression of HER2-positive breast cancer.

methodsMouse cell lines MMTV-neu, HC-11 and COMMA-D, as well as human cell lines MCF10A, SKBR3, HCC1954 and BT474 were used. Real-time PCR was used to quantify AREG expression and neutralizing antibodies were used to reduce the autocrine/paracrine effects of AREG. Transfections using siRNA and shRNA were used to knockdown AREG expression in the cancer cell lines. Free-floating sphere formation, colony forming, scratch wound and Transwell assays were used to assess the proliferation, tumor forming and migratory capacities of transfected cancer cells.

resultsWe found AREG expression in both normal epithelial cell lines and tumor-derived cell lines. Knockdown of AREG protein expression resulted in reduced sphere sizes and reduced sphere numbers in both mouse and human cancer cells that overexpress erbB2/HER2. AREG was found to be involved in cancer cell migration and invasion. In addition, we found that AREG expression knockdown resulted in different migration capacities in normal and erbB2/HER2 overexpressing cancer cells.

conclusionsBased on our results we conclude that AREG is involved in regulating the proliferation and migration of erbB2/HER2-positive breast cancer cells.

Indexed as

AmphiregulinAnimalsBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticErb-b2 Receptor Tyrosine KinasesGene Expression Regulation, NeoplasticHumansMiceRNA, Small InterferingAmphiregulinERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesRNA, Small InterferingAmphiregulinBreast cancererbB2HER2MigrationTransfection

Identifiers

PMID29181633
PMCPMC12995219
OpenAlexW2768332833

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.