Evidence map›Paper›PMID 39404181›Full record

ArticleMolecular oncology2025

Unraveling the metastasis-preventing effect of miR-200c in vitro and in vivo.

Bianca Köhler, Emily Brieger, Tom Brandstätter, Elisa Hörterer, Ulrich Wilk, Jana Pöhmerer, Anna Jötten, Philipp Paulitschke, Chase P Broedersz, Stefan Zahler and 3 more

Abstract read
In one paragraph

Article in Molecular oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

2 citing papers in PubMed.

  1. Article
  2. Article
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

13 authors.

Bianca KöhlerPharmaceutical Biotechnology, Department of Pharmacy, Ludwig-Maximilians-Universität München, Germany.
Emily BriegerFaculty of Physics and Center for NanoScience, Ludwig-Maximilians-Universität München, Germany.
Tom BrandstätterDepartment of Physics and Astronomy, Vrije Universiteit Amsterdam, The Netherlands.
Elisa HörtererPharmaceutical Biotechnology, Department of Pharmacy, Ludwig-Maximilians-Universität München, Germany.
Ulrich WilkPharmaceutical Biotechnology, Department of Pharmacy, Ludwig-Maximilians-Universität München, Germany.
Jana PöhmererPharmaceutical Biotechnology, Department of Pharmacy, Ludwig-Maximilians-Universität München, Germany.
Anna JöttenFaculty of Physics and Center for NanoScience, Ludwig-Maximilians-Universität München, Germany.
Philipp PaulitschkeFaculty of Physics and Center for NanoScience, Ludwig-Maximilians-Universität München, Germany.
Chase P BroederszDepartment of Physics and Astronomy, Vrije Universiteit Amsterdam, The Netherlands.
Stefan ZahlerPharmaceutical Biology, Department of Pharmacy, Ludwig-Maximilians-Universität München, Germany.
Joachim O RädlerFaculty of Physics and Center for NanoScience, Ludwig-Maximilians-Universität München, Germany.
Ernst WagnerPharmaceutical Biotechnology, Department of Pharmacy, Ludwig-Maximilians-Universität München, Germany.
Andreas RoidlPharmaceutical Biotechnology, Department of Pharmacy, Ludwig-Maximilians-Universität München, Germany.ORCID https://orcid.org/0000-0002-7629-1225

Funding

Deutsche Forschungsgemeinschaft 201269156 Collaborative Research Center SFB 1032
6 · The paper itself

Abstract

Advanced breast cancer, as well as ineffective treatments leading to surviving cancer cells, can result in the dissemination of these malignant cells from the primary tumor to distant organs. Recent research has shown that microRNA 200c (miR-200c) can hamper certain steps of the invasion-metastasis cascade. However, it is still unclear whether miR-200c expression alone is sufficient to prevent breast cancer cells from metastasis formation. Hence, we performed a xenograft mouse experiment with inducible miR-200c expression in MDA-MB 231 cells. The ex vivo analysis of metastatic sites in a multitude of organs, including lung, liver, brain, and spleen, revealed a dramatically reduced metastatic burden in mice with miR-200c-expressing tumors. A fundamental prerequisite for metastasis formation is the motility of cancer cells and, therefore, their migration. Consequently, we analyzed the effect of miR-200c on collective- and single-cell migration in vitro, utilizing MDA-MB 231 and MCF7 cell systems with genetically modified miR-200c expression. Analysis of collective-cell migration revealed confluence-dependent motility of cells with altered miR-200c expression. Additionally, scratch assays showed an enhanced predisposition of miR-200c-negative cells to leave cell clusters. The in-between stage of collective- and single-cell migration was validated using transwell assays, which showed reduced migration of miR-200c-positive cells. Finally, to measure migration at the single-cell level, a novel assay on dumbbell-shaped micropatterns was performed, which revealed that miR-200c critically determines confined cell motility. All of these results demonstrate that sole expression of miR-200c impedes metastasis formation in vivo and migration in vitro and highlights miR-200c as a metastasis suppressor in breast cancer.

Indexed as

Breast NeoplasmsMicroRNAsNeoplasm MetastasisAnimalsCell Line, TumorCell MovementFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsMiceMicroRNAsMIRN200 microRNA, humanbreast cancermetastasismicroRNAmigrationmiR‐200c

Identifiers

PMID39404181
PMCPMC11977663

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Registered trials

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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.