Evidence map›Paper›PMID 40708945›Full record

ArticleFrontiers in oncology2025

Lamins regulate cancer cell plasticity and chemosensitivity.

Guofang Chen, Tingyi Wei, Ao Huang, Junwei Shen, Furong Ju, Shichao Huang, Haisen Li

Abstract read
In one paragraph

Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
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

7 authors.

Guofang Chen *Shanghai Key Laboratory of Maternal Fetal Medicine, Clinical and Translational Research Center of Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, China.
Tingyi Wei *Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Ao HuangShanghai Key Laboratory of Maternal Fetal Medicine, Clinical and Translational Research Center of Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, China.
Junwei ShenClinical Research Center for Mental Disorders, Shanghai Pudong New Area Mental Health Center, School of Medicine, Tongji University, Shanghai, China.
Furong JuDepartment of Biomedical Sciences, Jockey Club College of Veterinary Medicine and Life Sciences, The Tung Biomedical Sciences Centre, City University of Hong Kong, Hong Kong, Hong Kong SAR, China.
Shichao HuangState Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, China.
Haisen LiShanghai Key Laboratory of Maternal Fetal Medicine, Clinical and Translational Research Center of Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Stem cell plasticity plays key roles in mammalian organogenesis, tissue homeostasis, and carcinogenesis. Given its tolerance to anti-tumor therapy and its promotion on immunosuppressive microenvironment, cancer cell plasticity is a major contributor to cancer recurrence and metastasis. It is necessary to explore novel avenues to resolve the limitations of current treatments. Methods: We established stable cancer cell lines harboring all lamin knockdown and then explored the effects of all lamin deficiency on cancer plasticity and tumorigenesis in both cell and subcutaneous mouse models. Results: We found that all lamin knockdown disrupts cancer cell plasticity and impairs tumor progression. The deficiency of all lamin subtypes impaired the stemness and cell cycle transition of cancer cell. Lamin knockdown modulated genomic damage and repair pathways, inhibited mitochondrial function, and triggered cellular senescence. Moreover, lamin knockdown within cancer cell suppressed cancer growth Conclusions: Overall, our findings characterize the significance of nuclear lamins in cancer cell plasticity and offer an attractive way to improve the effectiveness of anti-cancer therapy.

Indexed as

cancer cell plasticitychemosensitivityHIF-1 signalinglaminPD-L1

Identifiers

PMID40708945
PMCPMC12286797

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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.