Evidence map›Paper›PMID 35896617›Full record

ArticleOncogene2022

Low lamin A levels enhance confined cell migration and metastatic capacity in breast cancer.

Emily S Bell, Pragya Shah, Noam Zuela-Sopilniak, Dongsung Kim, Alice-Anais Varlet, Julien L P Morival, Alexandra L McGregor, Philipp Isermann, Patricia M Davidson, Juniper J Elacqua and 6 more

Open access · greenAbstract read
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 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
9.1field-weighted citation impact, top 1% 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

80 citing papers in PubMed, 117 citations in OpenAlex.

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  15. Amoeboid-mesenchymal transition and the proteolytic control of cancer invasion plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2026
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20 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

16 authors at 4 institutions in 2 countries.

Emily S BellWeill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, USA.
Pragya ShahWeill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, USA.
Noam Zuela-SopilniakWeill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, USA.
Dongsung KimWeill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, USA.
Alice-Anais VarletWeill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, USA.ORCID http://orcid.org/0000-0002-1670-4884
Julien L P MorivalWeill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, USA.ORCID http://orcid.org/0000-0003-1252-025X
Alexandra L McGregorWeill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, USA.
Philipp IsermannWeill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, USA.
Patricia M DavidsonWeill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, USA.
Juniper J ElacquaWeill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, USA.
Jonathan N LakinsCenter for Bioengineering and Tissue Regeneration, Department of Surgery, University of California San Francisco, San Francisco, CA, USA.
Linda VahdatDepartment of Medicine, Weill Cornell Medicine, New York, NY, USA.
Valerie M WeaverCenter for Bioengineering and Tissue Regeneration, Department of Surgery, University of California San Francisco, San Francisco, CA, USA.ORCID http://orcid.org/0000-0003-4786-6752
Marcus B SmolkaWeill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, USA.
Paul N SpanDepartment of Radiation Oncology, Radiotherapy & OncoImmunology laboratory, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.ORCID http://orcid.org/0000-0002-1930-6638
Jan LammerdingWeill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, USA. jan.lammerding@cornell.edu.ORCID http://orcid.org/0000-0003-4335-8611
Cornell University · USUniversity of California, San Francisco · USPennsylvania State University · USRadboud University Nijmegen · NL

Funding

Project 3: Single Cell Measures of Intratumor Diversity for Optimal Breast Cancer TherapyU54CA193461 · NCI · DANA-FARBER CANCER INST · PI MICHOR, FRANZISKA · 2015 to 2020
$11.2M
Project 3: Physical and Metabolic Constraints of Cancer Cell InvasionU54CA210184 · NCI · CORNELL UNIVERSITY · PI CANTLEY, LEWIS C., FISCHBACH, CLAUDIA · 2016 to 2020
$10.2M
Tissue mechanics reprograms the tissue to malignancy and metastasisR35CA242447 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI VALERIE MARIE WEAVER · 2020 to 2026
$6.6M
Nuclear mechanics and mechanotransduction in muscular laminopathiesR01HL082792 · NHLBI · CORNELL UNIVERSITY · PI LAMMERDING, JAN · 2007 to 2023
$4.8M
Signaling Mechanisms in Genome Maintenance (Equipment Supplement 2023)R35GM141159 · NIGMS · CORNELL UNIVERSITY · PI Marcus Smolka · 2021 to 2026
$3.5M
Nuclear mechanobiology in confined migration (Equipment Supplement 2023)R01GM137605 · NIGMS · CORNELL UNIVERSITY · PI LAMMERDING, JAN · 2020 to 2023
$1.6M
Mechanisms of heterochromatin replicationR01GM123018 · NIGMS · CORNELL UNIVERSITY · PI SMOLKA, MARCUS · 2018 to 2021
$1.2M
NCI NIH HHS R35 CA242447NCI NIH HHS U54 CA193461NCI NIH HHS U54 CA210184NHLBI NIH HHS R01 HL082792NIGMS NIH HHS R01 GM123018NIGMS NIH HHS R01 GM137605NIGMS NIH HHS R35 GM141159
6 · The paper itself

Abstract

Aberrations in nuclear size and shape are commonly used to identify cancerous tissue. However, it remains unclear whether the disturbed nuclear structure directly contributes to the cancer pathology or is merely a consequence of other events occurring during tumorigenesis. Here, we show that highly invasive and proliferative breast cancer cells frequently exhibit Akt-driven lower expression of the nuclear envelope proteins lamin A/C, leading to increased nuclear deformability that permits enhanced cell migration through confined environments that mimic interstitial spaces encountered during metastasis. Importantly, increasing lamin A/C expression in highly invasive breast cancer cells reflected gene expression changes characteristic of human breast tumors with higher LMNA expression, and specifically affected pathways related to cell-ECM interactions, cell metabolism, and PI3K/Akt signaling. Further supporting an important role of lamins in breast cancer metastasis, analysis of lamin levels in human breast tumors revealed a significant association between lower lamin A levels, Akt signaling, and decreased disease-free survival. These findings suggest that downregulation of lamin A/C in breast cancer cells may influence both cellular physical properties and biochemical signaling to promote metastatic progression.

Indexed as

Breast NeoplasmsLamin Type ACell MovementFemaleHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktLamin Type APhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID35896617
PMCPMC9925375
OpenAlexW4288051156

What OpenQuestion holds

Textmetadata
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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.