Evidence map›Paper›PMID 31430931›Full record

ArticleJournal of clinical medicine2019

Multi-Omics Characterization of the Spontaneous Mesenchymal-Epithelial Transition in the PMC42 Breast Cancer Cell Lines.

Sugandha Bhatia, James Monkman, Tony Blick, Pascal Hg Duijf, Shivashankar H Nagaraj, Erik W Thompson

Abstract read
In one paragraph

Article in Journal of clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Chromosomal instability and its effect on cell lines.Cancer reports (Hoboken, N.J.) · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Breast cancer metastasis: Is it a matter of OMICS and proper ex-vivo models?Computational and structural biotechnology journal · 2022
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. 'Omics Approaches to Explore the Breast Cancer Landscape.Frontiers in cell and developmental biology · 2019
    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

6 authors.

Sugandha BhatiaInstitute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD 4059, Australia. sugandha.bhatia@hdr.qut.edu.au.ORCID 0000-0003-3092-8283
James MonkmanInstitute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD 4059, Australia.
Tony BlickInstitute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD 4059, Australia.
Pascal Hg DuijfInstitute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD 4059, Australia.ORCID 0000-0001-8646-9843
Shivashankar H NagarajInstitute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD 4059, Australia.
Erik W ThompsonInstitute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD 4059, Australia. e2.thompson@qut.edu.au.ORCID 0000-0002-9723-4924

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal plasticity (EMP), encompassing epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET), are considered critical events for cancer metastasis. We investigated chromosomal heterogeneity and chromosomal instability (CIN) profiles of two sister PMC42 breast cancer (BC) cell lines to assess the relationship between their karyotypes and EMP phenotypic plasticity. Karyotyping by GTG banding and exome sequencing were aligned with SWATH quantitative proteomics and existing RNA-sequencing data from the two PMC42 cell lines; the mesenchymal, parental PMC42-ET cell line and the spontaneously epithelially shifted PMC42-LA daughter cell line. These morphologically distinct PMC42 cell lines were also compared with five other BC cell lines (MDA-MB-231, SUM-159, T47D, MCF-7 and MDA-MB-468) for their expression of EMP and cell surface markers, and stemness and metabolic profiles. The findings suggest that the epithelially shifted cell line has a significantly altered ploidy of chromosomes 3 and 13, which is reflected in their transcriptomic and proteomic expression profiles. Loss of the TGFβR2 gene from chromosome 3 in the epithelial daughter cell line inhibits its EMT induction by TGF-β stimulus. Thus, integrative 'omics' characterization established that the PMC42 system is a relevant MET model and provides insights into the regulation of phenotypic plasticity in breast cancer.

Indexed as

copy number variations (CNV)epithelial–mesenchymal transition (EMT)karyotypingmesenchymal–epithelial transition (MET)metabolismproteomicsRNA-sequencingseahorse extracellular flux analyserwhole exome sequencing

Identifiers

PMID31430931
PMCPMC6723942

What OpenQuestion holds

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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.