Evidence map›Paper›PMID 28724911›Full record

ArticleScientific reports2017

Honokiol inhibits c-Met-HO-1 tumor-promoting pathway and its cross-talk with calcineurin inhibitor-mediated renal cancer growth.

Murugabaskar Balan, Samik Chakraborty, Evelyn Flynn, David Zurakowski, Soumitro Pal

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. 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
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

24 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Navigating the redox landscape: reactive oxygen species in regulation of cell cycle.Redox report : communications in free radical research · 2024
    Review
  4. Review
  5. Review
  6. Review
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  9. Article
  10. Effects ofThe Journal of international medical research · 2022
    Article
  11. Review
  12. Review
  13. Metabolic reprogramming in renal cancer: Events of a metabolic disease.Biochimica et biophysica acta. Reviews on cancer · 2021
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
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  20. 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

5 authors at 2 institutions in 1 country.

Murugabaskar BalanDivision of Nephrology, Boston Children's Hospital, Boston, MA, 02115, United States.
Samik ChakrabortyDivision of Nephrology, Boston Children's Hospital, Boston, MA, 02115, United States.
Evelyn FlynnDivision of Nephrology, Boston Children's Hospital, Boston, MA, 02115, United States.
David ZurakowskiDepartment of Anesthesia, Boston Children's Hospital, Boston, MA, 02115, United States.
Soumitro PalDivision of Nephrology, Boston Children's Hospital, Boston, MA, 02115, United States. soumitro.pal@childrens.harvard.edu.
Harvard University · USBoston Children's Hospital · US

Funding

Novel Role(s) of Nrf2 in the Growth of Post-Transplantation CancerR01CA193675 · NCI · BOSTON CHILDREN'S HOSPITAL · PI PAL, SOUMITRO · 2016 to 2020
$2.0M
Novel Role of Honokiol in Preventing Cancer during Immune SuppressionR21CA191735 · NCI · BOSTON CHILDREN'S HOSPITAL · PI PAL, SOUMITRO · 2015 to 2016
$435k
NCI NIH HHS R01 CA193675NCI NIH HHS R21 CA191735
6 · The paper itself

Abstract

Honokiol (HNK) is a small molecule with potent anti-inflammatory and anti-tumorigenic properties; yet the molecular targets of HNK are not well studied. Hyperactivation of the receptor tyrosine kinase c-Met and overexpression of the cytoprotective enzyme heme oxygenase-1 (HO-1) play a critical role in the growth and progression of renal cell carcinoma (RCC). Interestingly, the calcineurin inhibitor (CNI) cyclosporine A (CsA), an immunosuppressant used to prevent allograft rejection, can also increase the risk of RCC in transplant patients. We studied the potential role of c-Met signaling axis on CNI-induced renal tumor growth and tested the anti-tumor efficacy of HNK. Importantly, CNI treatment promoted c-Met induction and enhanced c-Met-induced Ras activation. We found that HNK treatment effectively down-regulated both c-Met phosphorylation and Ras activation in renal cancer cells. It inhibited the expression of both c-Met- and CNI-induced HO-1, and promoted cancer cell apoptosis. In vivo, HNK markedly inhibited CNI-induced renal tumor growth; and it decreased the expression of phospho-c-Met and HO-1 and reduced blood vessel density in tumor tissues. Our results suggest a novel mechanism(s) by which HNK exerts its anti-tumor activity through the inhibition of c-Met-Ras-HO-1 axis; and it can have significant therapeutic potential to prevent post-transplantation cancer in immunosuppressed patients.

Indexed as

Allyl CompoundsAnimalsApoptosisBiphenyl CompoundsCalcineurin InhibitorsCell Line, TumorCell MovementCell ProliferationCell SurvivalDown-RegulationHeme Oxygenase-1Hepatocyte Growth FactorHumansHuman Umbilical Vein Endothelial CellsKidney NeoplasmsLignansAllyl CompoundsBiphenyl CompoundsCalcineurin InhibitorsHeme Oxygenase-1Hepatocyte Growth FactorhonokiolLignansMET protein, humanPhenolsProto-Oncogene Proteins c-metras Proteins

Identifiers

PMID28724911
PMCPMC5517643
OpenAlexW2734814397

What OpenQuestion holds

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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.