Evidence map›Paper›PMID 30043217›Full record

ArticleJournal of natural medicines2018

Bioassay-guided isolation of cantharidin from blister beetles and its anticancer activity through inhibition of epidermal growth factor receptor-mediated STAT3 and Akt pathways.

Jaemoo Chun, Min Kyoung Park, Hyejin Ko, Kyungjin Lee, Yeong Shik Kim

Abstract read
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In one paragraph

Article in Journal of natural medicines, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 33% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. STAT3 as a potential therapeutic target in triple negative breast cancer: a systematic review.Journal of experimental & clinical cancer research : CR · 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

5 authors at 2 institutions in 3 countries.

Jaemoo ChunNatural Products Research Institute, College of Pharmacy, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, South Korea.
Min Kyoung ParkNatural Products Research Institute, College of Pharmacy, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, South Korea.
Hyejin KoNatural Products Research Institute, College of Pharmacy, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, South Korea.
Kyungjin LeeDepartment of Herbology, College of Korean Medicine, Kyung Hee University, Seoul, 02447, South Korea.
Yeong Shik KimNatural Products Research Institute, College of Pharmacy, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, South Korea. kims@snu.ac.kr.ORCID http://orcid.org/0000-0003-1353-3925
Seoul National University · KRKyung Hee University · KR

Funding

MRC grant from the National Research Foundation of Korea 2009-0083533
6 · The paper itself

Abstract

Cantharidin is an active constituent of blister beetles (cantharides) which have traditionally been used for cancer treatment. Several studies have shown that cantharidin has a cytotoxic effect on various cancer cells. However, few studies have examined the effect of cantharidin on signal transducer and activator of transcription 3 (STAT3) signaling in cancer. In this study, we isolated cantharidin from cantharides by bioassay-guided fractionation and examined its inhibitory effect on STAT3 activation in human breast cancer MDA-MB-231 cells, expressing high level of phosphorylated STAT3. Cantharides were extracted with acetonitrile and separated into hexane, methylene chloride/acetonitrile, and water fractions. The methylene chloride/acetonitrile fraction was further separated into four fractions by preparative high-throughput high-performance liquid chromatography. Cantharidin was then isolated from the third fraction by countercurrent chromatography and structurally determined by comparing nuclear magnetic resonance and high-resolution mass spectrometry data. Cantharidin inhibited STAT3 tyrosine phosphorylation in MDA-MB-231 cells. Cantharidin suppressed epidermal growth factor (EGF)-induced STAT3 and PI3K/Akt signaling pathways through inhibition of EGF receptor phosphorylation. Moreover, cantharidin reduced cell proliferation and induced apoptosis with downregulation of STAT3 target genes, such as Bcl-2, COX-2, and cyclin D

Indexed as

AnimalsAntineoplastic AgentsCantharidinColeopteraErbB ReceptorsHumansProto-Oncogene Proteins c-aktSignal TransductionSTAT3 Transcription FactorAntineoplastic AgentsCantharidinErbB ReceptorsProto-Oncogene Proteins c-aktSTAT3 protein, humanSTAT3 Transcription FactorAktBioassay-guided isolationCantharidinEGFRMDA-MB-231 cellsSTAT3

Identifiers

PMID30043217
OpenAlexW2883437715

What OpenQuestion holds

Textmetadata
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.