Evidence map›Paper›PMID 28624442›Full record

ArticleToxicology and applied pharmacology2017

Loss of fructose-1,6-bisphosphatase induces glycolysis and promotes apoptosis resistance of cancer stem-like cells: an important role in hexavalent chromium-induced carcinogenesis.

Jin Dai, Yanli Ji, Wei Wang, Donghern Kim, Leonard Yenwong Fai, Lei Wang, Jia Luo, Zhuo Zhang

Open access · greenAbstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 49 citations in OpenAlex.

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  18. Environmental exposures, stem cells, and cancer.Pharmacology & therapeutics · 2019
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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

8 authors at 1 institution in 1 country.

Jin DaiDepartment of Toxicology and Cancer Biology, 1095 Veterans Drive, University of Kentucky, Lexington, KY 40536, USA.
Yanli JiDepartment of Toxicology and Cancer Biology, 1095 Veterans Drive, University of Kentucky, Lexington, KY 40536, USA.
Wei WangDepartment of Toxicology and Cancer Biology, 1095 Veterans Drive, University of Kentucky, Lexington, KY 40536, USA.
Donghern KimDepartment of Toxicology and Cancer Biology, 1095 Veterans Drive, University of Kentucky, Lexington, KY 40536, USA.
Leonard Yenwong FaiDepartment of Toxicology and Cancer Biology, 1095 Veterans Drive, University of Kentucky, Lexington, KY 40536, USA.
Lei WangCenter for Research on Environmental Diseases, 1095 Veterans Drive, University of Kentucky, Lexington, KY 40536, USA.
Jia LuoDepartment of Pharmacology and Nutritional Sciences, 1095 Veterans Drive, University of Kentucky, Lexington, KY 40536, USA.
Zhuo ZhangDepartment of Toxicology and Cancer Biology, 1095 Veterans Drive, University of Kentucky, Lexington, KY 40536, USA. Electronic address: zhuo.zhang@uky.edu.
University of Kentucky · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI KATHLEEN L. O'CONNOR · 2013 to 2026
$38.3M
Apoptosis resistance and Cr(VI) carcinogenesisR01ES021771 · NIEHS · UNIVERSITY OF KENTUCKY · PI SHI, XIANGLIN, ZHANG, ZHUO · 2014 to 2018
$1.7M
NCI NIH HHS P30 CA177558NIEHS NIH HHS R01 ES021771
6 · The paper itself

Abstract

Hexavalent chromium (Cr(VI)) compounds are confirmed human carcinogens for lung cancer. Our previous studies has demonstrated that chronic exposure of human bronchial epithelial BEAS-2B cells to low dose of Cr(VI) causes malignant cell transformation. The acquisition of cancer stem cell-like properties is involved in the initiation of cancers. The present study has observed that a small population of cancer stem-like cells (BEAS-2B-Cr-CSC) exists in the Cr(VI)-transformed cells (BEAS-2B-Cr). Those BEAS-2B-Cr-CSC exhibit extremely reduced capability of generating reactive oxygen species (ROS) and apoptosis resistance. BEAS-2B-Cr-CSC are metabolic inactive as evidenced by reductions in oxygen consumption, glucose uptake, ATP production, and lactate production. Most importantly, BEAS-2B-Cr-CSC are more tumorigenic with high levels of cell self-renewal genes, Notch1 and p21. Further study has found that fructose-1,6-bisphosphatase (FBP1), an rate-limiting enzyme driving glyconeogenesis, was lost in BEAS-2B-Cr-CSC. Forced expression of FBP1 in BEAS-2B-Cr-CSC restored ROS generation, resulting in increased apoptosis, leading to inhibition of tumorigenesis. In summary, the present study suggests that loss of FBP1 is a critical event in tumorigenesis of Cr(VI)-transformed cells.

Indexed as

AnimalsApoptosisCarcinogenesisCell LineCell Line, TransformedChromiumEpithelial CellsFructose-1,6-Diphosphatase DeficiencyFructose-BisphosphataseGlycolysisHumansMiceMice, NudeNeoplastic Stem CellsRespiratory MucosaChromiumchromium hexavalent ionFructose-BisphosphataseCancer stem cellsCr(VI)Fructose-1,6-bisphosphataseMetabolismReactive oxygen speciesTumorigenesis

Identifiers

PMID28624442
PMCPMC5567692
OpenAlexW2625708429

What OpenQuestion holds

Textmetadata
LicenceTDM
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.