Evidence map›Paper›PMID 28460475›Full record

ArticleOncotarget2017

Triptolide suppresses the in vitro and in vivo growth of lung cancer cells by targeting hyaluronan-CD44/RHAMM signaling.

Jung Min Song, Kalkidan Molla, Arunkumar Anandharaj, Ingrid Cornax, M Gerard O Sullivan, Ameya R Kirtane, Jayanth Panyam, Fekadu Kassie

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.7field-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

38 citing papers in PubMed, 56 citations in OpenAlex.

  1. HmmrResearch (Washington, D.C.) · 2026
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  11. Prospective bacterial and fungal sources of hyaluronic acid: A review.Computational and structural biotechnology journal · 2022
    Review
  12. A worldwide bibliometric analysis of triptolide research from 1997 to 2021.American journal of translational research · 2022
    Article
  13. Review
  14. 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

8 authors at 2 institutions in 1 country.

Jung Min SongMasonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
Kalkidan MollaMasonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
Arunkumar AnandharajMasonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
Ingrid CornaxMasonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
M Gerard O SullivanMasonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
Ameya R KirtaneDepartment of Pharmaceutics, University of Minnesota, Minneapolis, MN 55455, USA.
Jayanth PanyamDepartment of Pharmaceutics, University of Minnesota, Minneapolis, MN 55455, USA.
Fekadu KassieMasonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
University of Minnesota · USUniversity of Minnesota Medical Center · 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

Higher levels of hyaluronan (HA) and its receptors CD44 and RHAMM have been associated with poor prognosis and metastasis in NSCLC. In the current study, our goal was to define, using cellular and orthotopic lung tumor models, the role of HA-CD44/RHAMM signaling in lung carcinogenesis and to assess the potential of triptolide to block HA-CD44/RHAMM signaling and thereby suppress the development and progression of lung cancer. Triptolide reduced the viability of five non-small cell lung cancer (NSCLC) cells, the proliferation and self-renewal of pulmospheres, and levels of HA synthase 2 (HAS2), HAS3, HA, CD44, RHAMM, EGFR, Akt and ERK, but increased the cleavage of caspase 3 and PARP. Silencing of HAS2, CD44 or RHAMM induced similar effects. Addition of excess HA to the culture media completely abrogated the effects of triptolide and siRNAs targeting HAS2, CD44, or RHAMM. In an orthotopic lung cancer model in nude rats, intranasal administration of liposomal triptolide (400 μg/kg) for 8 weeks significantly reduced lung tumor growth as determined by bioluminescence imaging, lung weight measurements and gross and histopathological analysis of tumor burden. Also, triptolide suppressed expressions of Ki-67, a marker for cell proliferation, HAS2, HAS3, HA, CD44, and RHAMM in lung tumors. Overall, our results provide a strong rationale for mitigating lung cancer by targeting the HA-CD44/RHAMM signaling axis.

Indexed as

AnimalsAntineoplastic Agents, AlkylatingApoptosisCell Line, TumorCell MovementCell ProliferationCell SurvivalDisease Models, AnimalDiterpenesEpoxy CompoundsExtracellular Matrix ProteinsGene SilencingHumansHyaluronan ReceptorsHyaluronan SynthasesLung NeoplasmsAntineoplastic Agents, AlkylatingCD44 protein, humanDiterpenesEpoxy CompoundsExtracellular Matrix Proteinshyaluronan-mediated motility receptorHyaluronan ReceptorsHyaluronan SynthasesPhenanthrenesRNA, Small Interferingtriptolidehyaluronanhyaluronan receptorNSCLCorthotopictriptolide

Identifiers

PMID28460475
PMCPMC5432308
OpenAlexW2594423124

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.