Evidence map›Paper›PMID 27119349›Full record

ArticleOncotarget2016

Folate deficient tumor microenvironment promotes epithelial-to-mesenchymal transition and cancer stem-like phenotypes.

Yen-Hao Su, Wen-Chien Huang, Tse-Hung Huang, Yan-Jiun Huang, Yu-Kai Sue, Thanh-Tuan Huynh, Michael Hsiao, Tsan-Zon Liu, Alexander Th Wu, Chien-Min Lin

Abstract read
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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Review
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  15. Liver research (Beijing, China) · 2020
    Article
  16. Article
  17. Review
  18. Article
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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

10 authors.

Yen-Hao SuDepartment of Surgery, Division of General Surgery, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan.
Wen-Chien HuangInstitute of Traditional Medicine, School of Medicine, National Yang Ming University, Taipei, Taiwan.
Tse-Hung HuangDepartment of Traditional Chinese Medicine, Chang Gung Memorial Hospital, Keelung, Taiwan.
Yan-Jiun HuangDepartment of Surgery, Division of General Surgery, Taipei Medical University Hospital, Taipei, Taiwan.
Yu-Kai SueDepartment of Neurosurgery, Taipei Medical University-Shuang Ho Hospital, Taipei, Taiwan.
Thanh-Tuan HuynhCenter for Molecular Biomedicine, University of Medicine and Pharmacy, HoChiMinh City, Vietnam.
Michael HsiaoGenomics Research Center, Academia Sinica, Nankang, Taipei, Taiwan.
Tsan-Zon LiuTranslational Research Laboratory, Cancer Center, Taipei Medical University and Hospital, Taipei, Taiwan.
Alexander Th WuThe Ph.D. Program for Translational Medicine, College of Science and Technology, Taipei Medical University, Taipei, Taiwan.
Chien-Min LinDepartment of Neurosurgery, Taipei Medical University-Shuang Ho Hospital, Taipei, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clinically, serum level of folate has been negatively correlated to the stage and progression of liver cancer. Nevertheless, the functional consequence of folate deficiency (FD) in malignancy has not been fully investigated. Human hepatocellular carcinoma (HCC) cells (as study model) and other cancer types such as lung and glioma were cultured under folate deficient (FD) and folate complete (FD) conditions. Molecular characterization including intracellular ROS/RNS (reactive oxygen/nitrogen species), viability, colony formation, cancer stem-like cell (CSC) phenotype analyses were performed. In vivo tumorigenesis under FD and FC conditions were also examined. FD induced a significant increase in ROS and RNS, suppressing proliferative ability but inducing metastatic potential. Mesenchymal markers such as Snail, ZEB2, and Vimentin were significantly up-regulated while E-cadherin down-regulated. Importantly, CSC markers such as Oct4, β-catenin, CD133 were induced while PRRX1 decreased under FD condition. Furthermore, FD-conditioned HCC cells showed a decreased miR-22 level, leading to the increased expression of its target genes including HDAC4, ZEB2 and Oct4. Finally, xenograft mouse model demonstrated that FD diet promoted tumorigenesis and metastasis as compared to their FC counterparts. Our data provides rationales for the consideration of folate supplement as a metastasis preventive measure.

Indexed as

Epithelial-Mesenchymal TransitionTumor MicroenvironmentAnimalsCell Line, TumorCell ProliferationCell SurvivalFolic AcidFolic Acid DeficiencyGene Expression Regulation, NeoplasticHumansMice, Inbred NODMice, SCIDMicroRNAsNeoplasmsNeoplastic Stem CellsNitrosative StressFolic AcidMicroRNAsMIRN22 microRNA, humanReactive Nitrogen SpeciesReactive Oxygen Speciescancer stem-like cellsepithelial-mesenchymal transitionfolate deficiencymiR-22oxidative/nitrosative stress

Identifiers

PMID27119349
PMCPMC5078091

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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.