Evidence map›Paper›PMID 28618452›Full record

ArticleCell proliferation2017

Murine melanoma cells incomplete reprogramming using non-viral vector.

D A D Câmara, A S Porcacchia, A S Costa, R A Azevedo, I Kerkis

Abstract read
In one paragraph

Article in Cell proliferation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Cellular Reprogramming-A Model for Melanoma Cellular Plasticity.International journal of molecular sciences · 2020
    Review
  5. Article
  6. 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

5 authors.

D A D CâmaraLaboratory of Genetics, Butantan Institute, Sao Paulo, SP, Brazil.
A S PorcacchiaLaboratory of Genetics, Butantan Institute, Sao Paulo, SP, Brazil.
A S CostaLaboratory of Genetics, Butantan Institute, Sao Paulo, SP, Brazil.
R A AzevedoDepartament of Immunology, Laboratory of Tumor Immunology, Institute of Biomedical Science, University of Sao Paulo, Sao Paulo, SP, Brazil.
I KerkisLaboratory of Genetics, Butantan Institute, Sao Paulo, SP, Brazil.ORCID http://orcid.org/0000-0003-4433-7580

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThe reprogramming of cancer cells into induced pluripotent stem cells or less aggressive cancer cells can provide a modern platform to study cancer-related genes and their interactions with cell environment before and after reprogramming. Herein, we aimed to investigate the reprogramming capacity of murine melanoma B16F10 cells. MATERIALS AND

methodsThe B16F10 was transfected using non-viral circular DNA plasmid containing the genes Sox-2, Oct4, Nanog, Lin28 and green fluorescent protein (GFP). These cells were characterized by immunofluorescence, analysis RT-PCR and cell cycle.

resultsOur results demonstrated for the first time that reprogramming of B16F10 may be induced using non-viral minicircle DNA containing the four reprogramming factors Oct4, Sox2, Lin 28, Nanog (OSLN) and the GFP reporter gene. The resulting clones are composed by epithelioid cells. These cells display characteristics of cancer stem cells, thus expressing pluripotent stem cell markers and dividing asymmetrically and symmetrically. Reprogrammed B16F10 cells did not form teratomas; however, they showed the suppression of tumourigenic abilities characterized by a reduced tumour size, when compared with parental B16F10 cell line. In contrast to parental cell line that showed accumulation of the cells in S phase of cell cycle, the cells of reprogrammed clones are accumulated in G1 phase. Long-term cultivation of reprogrammed B16F10 cells induces regression of their reprogramming.

conclusionsOur data imply that in result of reprogramming of B16F10 cells less aggressive Murine Melanoma Reprogrammed Cancer Cells may be obtained. These cells represent an interesting model to study mechanism of cells malignancy as well as provide a novel tool for anti-cancer drugs screening.

Indexed as

Cellular ReprogrammingAnimalsCell Line, TumorG1 Phase Cell Cycle CheckpointsGenetic VectorsGreen Fluorescent ProteinsMelanoma, ExperimentalMiceMicroscopy, FluorescenceNanog Homeobox ProteinOctamer Transcription Factor-3Pluripotent Stem CellsRNA-Binding ProteinsSOXB1 Transcription FactorsGreen Fluorescent ProteinsNanog Homeobox ProteinOctamer Transcription Factor-3RNA-Binding ProteinsSOXB1 Transcription Factors

Identifiers

PMID28618452
PMCPMC6529082

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.