Evidence map›Paper›PMID 26871601›Full record

ArticleOncotarget2016

Acquisition of tumorigenic potential and enhancement of angiogenesis in pulmonary stem/progenitor cells through Oct-4 hyperexpression.

Sing-Yi Gu, Choa-Chi Ho, Yung-Kang Huang, Huei-Wen Chen, Yu-Chi Wang, Chia-Yu Kuo, Shu-Chun Teng, Wen-Mei Fu, Pan-Chyr Yang, Cheng-Wen Wu and 2 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 43% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

12 authors at 2 institutions in 1 country.

Sing-Yi GuGraduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Choa-Chi HoDepartment of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Yung-Kang HuangDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Huei-Wen ChenGraduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Yu-Chi WangDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Chia-Yu KuoDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Shu-Chun TengDepartment of Microbiology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Wen-Mei FuDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Pan-Chyr YangDepartment of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Cheng-Wen WuInstitute of Biomedical Science, Academia Sinica, Taipei, Taiwan.
Fu-Chuo PengGraduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Thai-Yen LingDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
National Taiwan University · TWInstitute of Biomedical Sciences, Academia Sinica · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer stem cells, also known as cancer initiating cells (CICs), are considered to be responsible for tumor growth and chemoresistance. Different hypotheses have been proposed to explain the origin of CICs, including mutations in adult stem/progenitor cells or the acquisition of stem-like characteristics in differentiated cells; however, studies have yielded conflicting identification for CICs and have little information for the origin to generate CICs. Part of the difficulty in identifying CICs may stem from the fact that the CICs studied have been largely derived from cancer cell lines or well-developed tumors. In previous studies, we have reported the enrichment of mouse pulmonary stem/progenitor cells (mPSCs) by using serum-free primary selection culture followed by FACS isolation using the coxsackievirus/adenovirus receptor (CAR) as the positive selection marker. Here, we demonstrated that overexpression of the pluripotent transcription factor Oct-4 is sufficient to induce CAR+/mPSCs transformation, which we name CAR+/mPSCsOct-4_hi. These transformed cells possess cancer initiating and chemoresistance potential, as well as exhibiting remarkable expression of certain proangiogenic factors, including angiopoietins (ANGs) and VEGF, and enhanced angiogenic potential. Moreover, CAR+/mPSCsOct-4_hi actively participated in tumor blood vessel formation and triggered a novel angiogenic mechanism, the angiopoietins/Tie2 signaling pathway. These study provide critical evidence supporting the possible origin to generate CICs, and help elucidate the pathways responsible for CICs-mediated blood vessel formation.

Indexed as

AdenocarcinomaAnimalsApoptosisBiomarkers, TumorCarcinogenesisCell ProliferationHumansLung NeoplasmsMaleMiceMice, SCIDNeoplastic Stem CellsNeovascularization, PathologicOctamer Transcription Factor-3Tumor Cells, CulturedXenograft Model Antitumor AssaysBiomarkers, TumorOctamer Transcription Factor-3POU5F1 protein, humanangiogenesisangiopoietins/Tie2cancer initiating cellsOct-4pulmonary stem/progenitor cells

Identifiers

PMID26871601
PMCPMC4924688
OpenAlexW2291711269

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.