Evidence map›Paper›PMID 25342300›Full record

ArticleBMC pharmacology & toxicology2014

Nobiletin suppresses cell viability through AKT pathways in PC-3 and DU-145 prostate cancer cells.

Jianchu Chen, Ashley Creed, Allen Y Chen, Haizhi Huang, Zhaoliang Li, Gary O Rankin, Xingqian Ye, Guihua Xu, Yi Charlie Chen

Open access · goldAbstract read
In one paragraph

Article in BMC pharmacology & toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
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  13. Nobiletin as an inducer of programmed cell death in cancer: a review.Apoptosis : an international journal on programmed cell death · 2022
    Review
  14. Article
  15. Article
  16. The Application ofEvidence-based complementary and alternative medicine : eCAM · 2021
    Review
  17. Systematically Deciphering the Pharmacological Mechanism of Fructus Aurantii via Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2021
    Article
  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

9 authors at 4 institutions in 2 countries.

Jianchu Chen
Ashley Creed
Allen Y Chen
Haizhi Huang
Zhaoliang Li
Gary O Rankin
Xingqian Ye
Guihua Xu
Yi Charlie ChenCollege of Science, Technology and Mathematics, Alderson Broaddus University, Philippi, WV 26416, USA. chenyc@ab.edu.
Alderson Broaddus University · USZhejiang University · CNMarshall University · USWest Virginia University · US

Funding

WV INBRE: The Inhibitor of Growth Family Member 4 (ING4) inhibits L-Type Amino Acid Transporter 1 (LAT1) expression to suppress Breast CancerP20GM103434 · NIGMS · MARSHALL UNIVERSITY · PI Travis Salisbury · 2012 to 2026
$61.1M
WVU &MU NEW FACULTY GRANTSP20RR016477 · NCRR · MARSHALL UNIVERSITY · PI RANKIN, GARY O · 2001 to 2011
$35.5M
NCRR NIH HHS 5P20RR016477NIGMS NIH HHS 8P20GM104434NIGMS NIH HHS P20 GM103434
6 · The paper itself

Abstract

backgroundNobiletin is a non-toxic dietary flavonoid that possesses anti-cancer properties. Nobiletin has been reported to reduce the risk of prostate cancer, but the mechanism is not well understood. In this study, we investigated the effects of nobiletin in prostate cancer cell lines PC-3 and DU-145.

methodsNobiletin was isolated from a polymethoxy flavonoid mixture using HPLC, cell viability was analyzed with MTS-based assays. Protein expression was examined by ELISA and western blotting. Gene expression was examined by luciferase assay. And the pathways were examined by manipulating genetic components with plasmid transfection.

resultsData showed that nobiletin decreased cell viability in both prostate cell lines, with a greater reduction in viability in PC-3 cells. HIF-1α expression and AKT phosphorylation were decreased in both cell lines. The VEGF expression was inhibited in PC-3 but not DU-145 cells. cMyc expression was decreased in DU-145 cells. Nobiletin down-regulated NF-κB (p50) expression in nuclei of DU145 cells but not whole cells. It also suppressed NF-κB expression in both whole cells and nuclei of PC-3 cells. Increasing HIF-1α levels reversed nobiletin's inhibitory effects on VEGF expression, and up-regulating AKT levels reversed its inhibitory effects on HIF-1α expression. We speculate that AKT influences cell viability probably by its effect on NF-κB in both prostate cells. The effect of nobiletin on VEGF expression in PC-3 cell lines was through the AKT/HIF-1α pathway.

conclusionTaken together, our results show that nobiletin suppresses cell viability through AKT pathways, with a more profound effect against the more metastatic PC-3 line. Due to this enhanced action against a more malignant cell type, nobiletin may be used to improve prostate cancer survival rates.

Indexed as

Blotting, WesternCell Line, TumorEnzyme-Linked Immunosorbent AssayFlavonesHumansHypoxia-Inducible Factor 1, alpha SubunitMaleNF-kappa BPhosphorylationProstatic NeoplasmsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycVascular Endothelial Growth Factor AFlavonesHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitNF-kappa BnobiletinProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycVascular Endothelial Growth Factor A

Identifiers

PMID25342300
PMCPMC4212237
OpenAlexW2067360604

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.