Evidence map›Paper›PMID 27458163›Full record

ArticleOncotarget2016

Honokiol suppresses lung tumorigenesis by targeting EGFR and its downstream effectors.

Jung Min Song, Arunkumar Anandharaj, Pramod Upadhyaya, Ameya R Kirtane, Jong-Hyuk Kim, Kwon Ho Hong, Jayanth Panyam, Fekadu Kassie

Open access · diamondAbstract 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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 37 citations in OpenAlex.

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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 2 institutions in 1 country.

Jung Min SongMasonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
Arunkumar AnandharajMasonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
Pramod UpadhyayaMasonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
Ameya R KirtaneDepartment of Pharmaceutics, University of Minnesota, Minneapolis, MN 55455, USA.
Jong-Hyuk KimMasonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
Kwon Ho HongInstitute for Therapeutics Discovery and Development, University of Minnesota, Minneapolis, MN 55414, USA.
Jayanth PanyamMasonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
Fekadu KassieMasonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
University of Minnesota Medical Center · USUniversity of Minnesota · US

Funding

Women's CancerP30CA077598 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Jeffrey S. Miller · 1998 to 2026
$100.4M
NCI NIH HHS P30 CA077598
6 · The paper itself

Abstract

Since epidermal growth factor receptor (EGFR) is commonly deregulated in pre-malignant lung epithelium, targeting EGFR may arrest the development of lung cancer. Here, we showed that honokiol (2.5-7.5 μM), a bioactive compound of Magnolia officinalis, differentially suppressed proliferation (up to 93%) and induced apoptosis (up to 61%) of EGFR overexpressing tumorigenic bronchial cells and these effects were paralleled by downregulation of phospho-EGFR, phospho-Akt, phospho-STAT3 and cell cycle-related proteins as early as 6-12 h post-treatment. Autocrine secretion of EGF sensitized 1170 cells to the effects of honokiol. Molecular docking studies indicated that honokiol binds to the tyrosine kinase domain of EGFR although it was less efficient than erlotinib. However, the anti-proliferative and pro-apoptotic activities of honokiol were stronger than those of erlotinib. Upon combinatory treatment, honokiol sensitized bronchial cells and erlotinib resistant H1650 and H1975 cells to erlotinib. Furthermore, in a mouse lung tumor bioassay, intranasal instillation of liposomal honokiol (5 mg/kg) for 14 weeks reduced the size and multiplicity (49%) of lung tumors and the level of total- and phospho-EGFR, phospho-Akt and phospho-STAT3. Overall, our results indicate that honokiol is a promising candidate to suppress the development and even progression of lung tumors driven by EGFR deregulation.

Indexed as

Allyl CompoundsAnimalsAntineoplastic Agents, PhytogenicApoptosisBiological AssayBiphenyl CompoundsBronchiCarcinogenesisCell CycleCell ProliferationCell SurvivalDisease ProgressionErbB ReceptorsErlotinib HydrochlorideFemaleLignans4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanoneAllyl CompoundsAntineoplastic Agents, PhytogenicBiphenyl CompoundsEGFR protein, humanErbB ReceptorsErlotinib HydrochloridehonokiolLignansNitrosaminesPhenolsPlant ExtractsRNA, Small Interfering4-(methylnitrosamino)-1-(3-pyridyl)-1-butanonechemopreventionEGFRhonokiollung tumor

Identifiers

PMID27458163
PMCPMC5295387
OpenAlexW2481421684

What OpenQuestion holds

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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.