Evidence map›Paper›PMID 28699810›Full record

ArticleCell cycle (Georgetown, Tex.)2017

A balanced level of profilin-1 promotes stemness and tumor-initiating potential of breast cancer cells.

Chang Jiang, Zhijie Ding, Marion Joy, Souvik Chakraborty, Su Hyeong Kim, Ralph Bottcher, John Condeelis, Shivendra Singh, Partha Roy

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 31% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Biomarkers of tumor invasiveness in proteomics (Review).International journal of oncology · 2020
    Pooled it
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  3. Article
  4. Article
  5. Review
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  7. Article
  8. Review
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  12. Review
  13. Profilin choreographs actin and microtubules in cells and cancer.International review of cell and molecular biology · 2020
    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

9 authors at 4 institutions in 2 countries.

Chang Jianga Bioengineering , University of Pittsburgh , PA , USA.
Zhijie Dinga Bioengineering , University of Pittsburgh , PA , USA.
Marion Joya Bioengineering , University of Pittsburgh , PA , USA.
Souvik Chakrabortya Bioengineering , University of Pittsburgh , PA , USA.
Su Hyeong Kimb University of Pittsburgh Cancer Institute , PA , USA.
Ralph Bottcherc Department of Molecular Medicine , Max-Planck Institute of Biochemistry , Martinsried , Germany.
John Condeelisd Anatomy and Structural Biology , Albert Einstein College of Medicine , Bronx , NY , USA.
Shivendra Singhb University of Pittsburgh Cancer Institute , PA , USA.
Partha Roya Bioengineering , University of Pittsburgh , PA , USA.
University of Pittsburgh · USUPMC Hillman Cancer Center · USAlbert Einstein College of Medicine · USMax Planck Institute of Biochemistry · DE

Funding

Signal transduction regulating tumor cell disseminationR01CA150344 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI CONDEELIS, JOHN S · 2010 to 2020
$3.7M
Profilin as a target to suppress Invasive breast cancerR01CA108607 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ROY, PARTHA · 2006 to 2017
$2.6M
Improving genomic prediction models in breast cancerR21CA108707 · NCI · DUKE UNIVERSITY · PI OLSON, JOHN A · 2004 to 2005
$277k
NCI NIH HHS R01 CA108607NCI NIH HHS R01 CA150344NCI NIH HHS R21 CA108707
6 · The paper itself

Abstract

Profilin-1 (Pfn1) is an important actin-regulatory protein that is downregulated in human breast cancer and when forcibly elevated, it suppresses the tumor-initiating ability of triple-negative breast cancer cells. In this study, we demonstrate that Pfn1 overexpression reduces the stem-like phenotype (a key biologic feature associated with higher tumor-initiating potential) of MDA-MB-231 (MDA-231) triple-negative breast cancer cells. Interestingly, the stem-like trait of MDA-231 cells is also attenuated upon depletion of Pfn1. A comparison of cancer stem cell gene (CSC) gene expression signatures between depleted and elevated conditions of Pfn1 further suggest that Pfn1 may be somehow involved in regulating the expression of a few CSC-related genes including MUC1, STAT3, FZD7, and ITGB1. Consistent with the reduced stem-like phenotype associated with loss-of-function of Pfn1, xenograft studies showed lower tumor-initiating frequency of Pfn1-depleted MDA-231 cells compared to their control counterparts. In MMTV:PyMT mouse model, homozygous but not heterozygous deletion of Pfn1 gene leads to severe genetic mosaicism and positive selection of Pfn1-proficient tumor cells further supporting the contention that a complete lack of Pfn1 is likely not conducive for efficient tumor initiation capability of breast cancer cells. In summary, these findings suggest that the maintenance of optimal stemness and tumor-initiating ability of breast cancer cells requires a balanced expression of Pfn1.

Indexed as

AnimalsCarcinogensCell Line, TumorGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateMiceMice, Inbred C57BLMice, KnockoutMucin-1Neoplastic Stem CellsProfilinsRNA InterferenceRNA, Small InterferingSTAT3 Transcription FactorTransplantation, HeterologousCarcinogensMUC1 protein, humanMucin-1ProfilinsRNA, Small InterferingSTAT3 protein, humanSTAT3 Transcription FactorBreast cancerProfilin1stemnesstumorigenicity

Identifiers

PMID28699810
PMCPMC5788419
OpenAlexW2734477466

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.