Evidence map›Paper›PMID 27609096›Full record

ArticleScientific reports2016

Paeoniflorin Potentiates the Inhibitory Effects of Erlotinib in Pancreatic Cancer Cell Lines by Reducing ErbB3 Phosphorylation.

Jian Hao, Xue Yang, Xiu-Li Ding, Lei-Ming Guo, Cui-Hong Zhu, Wei Ji, Tong Zhou, Xiong-Zhi Wu

Open access · goldAbstract readComparative Study
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. The Role and Mechanism ofMolecules (Basel, Switzerland) · 2024
    Review
  3. Article
  4. Article
  5. Intranasal delivery of paeoniflorin nanocrystals for brain targeting.Asian journal of pharmaceutical sciences · 2020
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
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 3 institutions in 2 countries.

Jian HaoZhong-Shan-Men Inpatient Department; National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy; Tianjin Medical University Cancer Institute and Hospital Tianjin, 300060, China.
Xue YangZhong-Shan-Men Inpatient Department; National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy; Tianjin Medical University Cancer Institute and Hospital Tianjin, 300060, China.
Xiu-Li DingZhong-Shan-Men Inpatient Department; National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy; Tianjin Medical University Cancer Institute and Hospital Tianjin, 300060, China.
Lei-Ming GuoClinical Immunology and Rheumatology, Medicine Department of University of Alabama at Birmingham, Birmingham, Alabama, USA.
Cui-Hong ZhuZhong-Shan-Men Inpatient Department; National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy; Tianjin Medical University Cancer Institute and Hospital Tianjin, 300060, China.
Wei JiOpening Cancer Laboratory, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China.
Tong ZhouClinical Immunology and Rheumatology, Medicine Department of University of Alabama at Birmingham, Birmingham, Alabama, USA.
Xiong-Zhi WuZhong-Shan-Men Inpatient Department; National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy; Tianjin Medical University Cancer Institute and Hospital Tianjin, 300060, China.
National Clinical Research · USTianjin Medical University Cancer Institute and Hospital · CNUniversity of Alabama at Birmingham · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Blockade of the epidermal growth factor receptor (EGFR) by EGFR tyrosine kinase inhibitors is insufficient for effective anti-tumor activity because the reactivation of the ErbB3 signaling pathway significantly contributes to activating the consequent phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. Combinatorial therapies including ErbB3 targeting may ameliorate tumor responses to anti-EGFR therapies. In the present study, we found that in BxPC-3 and L3.6pl cells, which highly expressed the ErbB3 receptor, significant reduction in cell viability, induction of apoptosis were observed when treated with a combination of erlotinib and PF compared to either agent alone. Moreover, in ErbB3-expressing BxPC-3, L3.6pl and S2VP10 cell lines, the inhibition of ErbB3/PI3K/Akt phosphorylation were observed when treated with PF. Most strikingly, both EGFR/MAPK/Erk and ErbB3/PI3K/Akt activitions were substantially suppressed when treated with the combination of PF and erlotinib. However, in the ErbB3-deficient cell line MIAPaCa-2, no such effects were observed with similar treatments. Most importantly, these in vitro results were replicated in nude mouse transplanted tumor models. Taken together, our findings show that PF enhances the effect of erlotinib in ErbB3-expressing pancreatic cancer cells by directly suppressing ErbB3 activation, and PF in combination with erlotinib is much more effective as an antitumor agent compared with either agent alone.

Indexed as

AnimalsCell Line, TumorCell ProliferationCell SurvivalDrug SynergismErlotinib HydrochlorideGene Expression Regulation, NeoplasticGlucosidesGlycosidesHumansMiceMice, NudeMonoterpenesPancreatic NeoplasmsPhosphorylationReceptor, ErbB-3ERBB3 protein, humanErlotinib HydrochlorideGlucosidesGlycosidesMonoterpenespeoniflorinReceptor, ErbB-3

Identifiers

PMID27609096
PMCPMC5016851
OpenAlexW2511133632

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.