Evidence map›Paper›PMID 27468690›Full record

ArticleCell death & disease2016

Tumorigenic potential is restored during differentiation in fusion-reprogrammed cancer cells.

J Yao, L Zhang, L Hu, B Guo, X Hu, U Borjigin, Z Wei, Y Chen, M Lv, J T Y Lau and 3 more

Abstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Generation of Cancer Stem/Initiating Cells by Cell-Cell Fusion.International journal of molecular sciences · 2022
    Review
  5. Review
  6. Article
  7. 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

13 authors.

J YaoDepartment of Cell Biology, Center for Stem Cells and Medicine, Second Military Medical University, Shanghai 200433, People's Republic of China.
L ZhangKey Laboratory of Molecular and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, People's Republic of China.
L HuDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xian 710061, People's Republic of China.
B GuoDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xian 710061, People's Republic of China.
X HuKey Laboratory of Molecular and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, People's Republic of China.
U BorjiginKey Laboratory of National Education Ministry for Mammalian Reproductive Biology and Biotechnology, Inner Mongolia University, Huhhot 010021, People's Republic of China.
Z WeiKey Laboratory of National Education Ministry for Mammalian Reproductive Biology and Biotechnology, Inner Mongolia University, Huhhot 010021, People's Republic of China.
Y ChenPearl Laboratory Animal Science and Technology Co. Ltd, Guangzhou, People's Republic of China.
M LvPearl Laboratory Animal Science and Technology Co. Ltd, Guangzhou, People's Republic of China.
J T Y LauDepartment of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.
X WangKey Laboratory of Molecular and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, People's Republic of China.
G LiKey Laboratory of National Education Ministry for Mammalian Reproductive Biology and Biotechnology, Inner Mongolia University, Huhhot 010021, People's Republic of China.
Y-P HuDepartment of Cell Biology, Center for Stem Cells and Medicine, Second Military Medical University, Shanghai 200433, People's Republic of China.

Funding

REGULATION OF LACTOSAMINYL GLYCAN BIOSYNTHESIS IN HEMATOPOIETIC CELLSP01HL107146 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI SACKSTEIN, ROBERT · 2011 to 2017
$17.7M
NHLBI NIH HHS P01 HL107146
6 · The paper itself

Abstract

Detailed understanding of the mechanistic steps underlying tumor initiation and malignant progression is critical for insights of potentially novel therapeutic modalities. Cellular reprogramming is an approach of particular interest because it can provide a means to reset the differentiation state of the cancer cells and to revert these cells to a state of non-malignancy. Here, we investigated the relationship between cellular differentiation and malignant progression by the fusion of four independent mouse cancer cell lines from different tissues, each with differing developmental potentials, to pluripotent mouse embryonic stem (ES) cells. Fusion was accompanied by loss of differentiated properties of the four parental cancer cell lines and concomitant emergence of pluripotency, demonstrating the feasibility to reprogram the malignant and differentiative properties of cancer cells. However, the original malignant and differentiative phenotypes re-emerge upon withdrawal of the fused cells from the embryonic environment in which they were maintained. cDNA array analysis of the malignant hepatoma progression implicated a role for Foxa1, and silencing Foxa1 prevented the re-emergence of malignant and differentiation-associated gene expression. Our findings support the hypothesis that tumor progression results from deregulation of stem cells, and our approach provides a strategy to analyze possible mechanisms in the cancer initiation.

Indexed as

Cell DifferentiationCellular ReprogrammingAdultAnimalsCarcinogenesisCell FusionCell Line, TumorDisease ProgressionEmbryonic Stem CellsHumansMice, TransgenicPhenotypePluripotent Stem CellsReproducibility of ResultsTeratomaTranscriptome

Identifiers

PMID27468690
PMCPMC4973342

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.