Evidence map›Paper›PMID 26068418›Full record

ArticleScientific reports2015

FoxO1-negative cells are cancer stem-like cells in pancreatic ductal adenocarcinoma.

Weifeng Song, Qi Li, Lei Wang, Weiyi Huang, Liwei Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

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  13. The adaptor protein CrkII regulates IGF-1-induced biological behaviors of pancreatic ductal adenocarcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  14. CCR7 regulates Twist to induce the epithelial-mesenchymal transition in pancreatic ductal adenocarcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  15. 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 at 1 institution in 1 country.

Weifeng Song1] Department of Medical Oncology, Shanghai First People's Hospital, Shanghai Jiao Tong University, Shanghai 200080, China [2] Shanghai Key Laboratory of Pancreatic Diseases Research, Shanghai 200080, China.
Qi Li1] Department of Medical Oncology, Shanghai First People's Hospital, Shanghai Jiao Tong University, Shanghai 200080, China [2] Shanghai Key Laboratory of Pancreatic Diseases Research, Shanghai 200080, China.
Lei WangDepartment of Medical Oncology, Shanghai First People's Hospital, Shanghai Jiao Tong University, Shanghai 200080, China.
Weiyi HuangDepartment of Medical Oncology, Shanghai First People's Hospital, Shanghai Jiao Tong University, Shanghai 200080, China.
Liwei Wang1] Department of Medical Oncology, Shanghai First People's Hospital, Shanghai Jiao Tong University, Shanghai 200080, China [2] Shanghai Key Laboratory of Pancreatic Diseases Research, Shanghai 200080, China.
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Flow cytometry assays using aldehyde dehydrogenase (ALDH) activity or CD133 positivity to isolate cancer stem cells (CSCs) are widely applied but have limitations. Thus, characterization of CSC makers for a specific cancer is potentially important. We have previously shown that miR-21 regulates cancer cell growth via FoxO1 in pancreatic ductal adenocarcinoma (PDAC). Here, we areported evidence of FoxO1-negative PDAC cells as CSCs in PDAC. Both ALDH-high and CD133-high cell fractions isolated from PDAC of the patients expressed high levels of miR-21 and null FoxO1. Cultured PDAC cells were virally transduced with GFP under FoxO1 promoter. GFP (FoxO1)-null PDAC cells expressed high levels of miR-21, and grew more quickly than FoxO1-positive PDAC cells. Moreover, the fold increases in growth of FoxO1-negative vs FoxO1-positive cells were greater than CD133-high vs CD133-low cells, or ALDH-high vs ALDH-low cells. Further, FoxO1-negative cells formed tumor spheres in culture and developed tumors after serial adoptive transplantation into NOD/SCID mice, while the FoxO1-positive cells did not. Finally, selective elimination of FoxO1-negative cells completely inhibited the growth of PDAC cells. Together, these data suggest that FoxO1-negative cells as CSCs in PDAC, and targeting FoxO1-negative cells in PDAC may provide better therapeutic outcome.

Indexed as

Carcinoma, Pancreatic DuctalForkhead Transcription FactorsMicroRNAsNeoplastic Stem CellsPancreatic NeoplasmsRNA, NeoplasmAnimalsCell Line, TumorForkhead Box Protein O1HeterograftsHumansMiceMice, Inbred NODMice, SCIDNeoplasm TransplantationForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanMicroRNAsMIRN21 microRNA, humanRNA, Neoplasm

Identifiers

PMID26068418
PMCPMC4464177
OpenAlexW2256076794

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.