Evidence map›Paper›PMID 23568779›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013

Passage-dependent cancerous transformation of human mesenchymal stem cells under carcinogenic hypoxia.

Spencer W Crowder, Linda W Horton, Sue Hyun Lee, Colt M McClain, Oriana E Hawkins, Amanda M Palmer, Hojae Bae, Ann Richmond, Hak-Joon Sung

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Passage dependence of NADH redox status and reactive oxygen species levelTranslational breast cancer research : a journal focusing on translational research in breast cancer · 2024
    Article
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  4. Regulation of CClHuman cell · 2019
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  17. Toxicogenomic effect of nickel and beyond.Archives of toxicology · 2014
    Review
  18. Review
  19. 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.

Spencer W CrowderDepartment of Biomedical Engineering, Vanderbilt University Medical Center, Nashville, Tennessee 37235, USA.
Linda W Horton
Sue Hyun Lee
Colt M McClain
Oriana E Hawkins
Amanda M Palmer
Hojae Bae
Ann Richmond
Hak-Joon Sung
Vanderbilt University Medical Center · USKyung Hee University · KRUnited States Department of Veterans Affairs · USVA Tennessee Valley Healthcare System · US

Funding

Integrated Biological Systems Training in OncologyT32CA119925 · NCI · VANDERBILT UNIVERSITY · PI Vivian Gama, William Patrick Tansey · 2008 to 2026
$7.6M
Targeting the NF-kappaB Pathway in MelanomaR01CA116021 · NCI · VANDERBILT UNIVERSITY · PI RICHMOND, ANN, YAN, CHI · 2005 to 2024
$6.7M
MELANOMA GROWTH STIMULATORY ACTIVITYR01CA034590 · NCI · VANDERBILT UNIVERSITY · PI RICHMOND, ANN · 1986 to 2017
$5.2M
Optimizing Bioactive Hydrogels to Control Angiogenesis and Inflammation in FunctiR21HL091465 · NHLBI · RUTGERS, THE STATE UNIV OF N.J. · PI KOHN, JOACHIM B. · 2009 to 2010
$425k
BIOCHEMIISTRY OF A MELANOMA GROWTH STIMULATIONR23CA034590 · NCI · EMORY UNIVERSITY · PI RICHMOND, ANN · 1985 to 1985
–
BLRD VA IK6 BX005225NCI NIH HHS CA34590-30NCI NIH HHS R01 CA034590NCI NIH HHS R01 CA116021NCI NIH HHS T32 CA119925NHLBI NIH HHS HL091465NHLBI NIH HHS R21 HL091465
6 · The paper itself

Abstract

Bone marrow-derived human mesenchymal stem cells (hMSCs) either promote or inhibit cancer progression, depending on factors that heretofore have been undefined. Here we have utilized extreme hypoxia (0.5% O2) and concurrent treatment with metal carcinogen (nickel) to evaluate the passage-dependent response of hMSCs toward cancerous transformation. Effects of hypoxia and nickel treatment on hMSC proliferation, apoptosis, gene and protein expression, replicative senescence, reactive oxygen species (ROS), redox mechanisms, and in vivo tumor growth were analyzed. The behavior of late passage hMSCs in a carcinogenic hypoxia environment follows a profile similar to that of transformed cancer cells (i.e., increased expression of oncogenic proteins, decreased expression of tumor suppressor protein, increased proliferation, decreased apoptosis, and aberrant redox mechanisms), but this effect was not observed in earlier passage control cells. These events resulted in accumulated intracellular ROS in vitro and excessive proliferation in vivo. We suggest a mechanism by which carcinogenic hypoxia modulates the activity of three critical transcription factors (c-MYC, p53, and HIF1), resulting in accumulated ROS and causing hMSCs to undergo cancer-like behavioral changes. This is the first study to utilize carcinogenic hypoxia as an environmentally relevant experimental model for studying the age-dependent cancerous transformation of hMSCs.

Indexed as

Cell Transformation, NeoplasticAnimalsBlotting, WesternCell DifferentiationCell HypoxiaCell ProliferationCells, CulturedDNA-Binding ProteinsFemaleForkhead Transcription FactorsGene ExpressionHumansHypoxia-Inducible Factor 1, alpha SubunitMesenchymal Stem CellsMiceMice, KnockoutDNA-Binding ProteinsForkhead Transcription FactorsHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMYCBP protein, humanNickelReactive Oxygen SpeciesTranscription FactorsTumor Suppressor Protein p53Whn proteinagingexperimental modelsp53reactive oxygen species

Identifiers

PMID23568779
PMCPMC3688746
OpenAlexW2141801963

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.