Evidence map›Paper›PMID 26173505›Full record

ArticleDigestive diseases and sciences2015

Trastuzumab Inhibits Growth of HER2-Negative Gastric Cancer Cells Through Gastrin-Initialized CCKBR Signaling.

Yan Cui, Shao-Bo Li, Xing-Chun Peng, Jun Wu, Guo-Hui Fu

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 13% 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, 18 citations in OpenAlex.

  1. Trial
  2. Article
  3. Potential Theranostic Roles of SLC4 Molecules in Human Diseases.International journal of molecular sciences · 2023
    Review
  4. CiberAMP: AnBiology · 2022
    Article
  5. Review
  6. Article
  7. Gastrin inhibits gastric cancer progression through activating the ERK-P65-miR23a/27a/24 axis.Journal of experimental & clinical cancer research : CR · 2018
    Article
  8. Article
  9. Article
  10. Article
  11. 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

5 authors at 2 institutions in 1 country.

Yan CuiDepartment of Oncology, Affiliated Hospital of Yanbian University, Yanbian, China.
Shao-Bo LiPathology Center, Shanghai First People's Hospital/Faculty of Basic Medicine, Shanghai Jiao Tong University School of Medicine, Number 280, South Chong-Qing Road, Shanghai, 200025, China.
Xing-Chun PengPathology Center, Shanghai First People's Hospital/Faculty of Basic Medicine, Shanghai Jiao Tong University School of Medicine, Number 280, South Chong-Qing Road, Shanghai, 200025, China.
Jun WuPathology Center, Shanghai First People's Hospital/Faculty of Basic Medicine, Shanghai Jiao Tong University School of Medicine, Number 280, South Chong-Qing Road, Shanghai, 200025, China. Jun.Wu@shsmu.edu.cn.
Guo-Hui FuPathology Center, Shanghai First People's Hospital/Faculty of Basic Medicine, Shanghai Jiao Tong University School of Medicine, Number 280, South Chong-Qing Road, Shanghai, 200025, China. guohuifu@shsmu.edu.cn.
Shanghai First People's Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAdministration of trastuzumab, a fully humanized monoclonal antibody targeted to the human epidermal growth factor receptor 2 (HER2, p185), has improved outcomes for patients with HER2-positive gastric cancer (GC), but some relevant issues remain to be investigated and will emerge with new anti-GC drugs. Gastrin is a major gastrointestinal hormone proven to have an inhibitory effect on GC in vitro and in vivo.

aimTo explore the sympathetic role of trastuzumab and gastrin on inhibition of GC.

methodsThe HER2-positive and HER2-negative GC cell lines were treated with trastuzumab, gastrin, or their combination in vitro and in xenograft model. The synergistical role of trastuzumab and gastrin and related mechanisms were investigated.

resultsWe found the synergistic inhibitory effects of trastuzumab and gastrin on HER2-negative GC cells through the gastrin/cholecystokinin B receptor (CCKBR) pathway. Trastuzumab upregulated CCKBR protein levels but could not initiate its signal transduction, whereas gastrin increased the levels and activation of CCKBR. Molecular experiments indicated that trastuzumab and gastrin co-treatment synergistically enhanced the stability of CCKBR. Moreover, their combined treatment synergistically arrested GC cells at G0/G1 phase, down-regulated levels of GC-related proteins, including anion exchanger 1 (AE1), cyclin D1, β-catenin, and cytoplasmic p16, and promoted nuclear translocation of p16. In addition, combination treatment upregulated AE2 levels, which are reduced in GC tissues. The in vivo synergistic anti-GC effect of combined treatment was confirmed in xenograft experiments.

conclusionsTrastuzumab plus gastrin inhibit growth of Her2-negative GC by targeting cytoplasmic AE1 and p16.

Indexed as

AnimalsAntineoplastic AgentsCell Line, TumorErb-b2 Receptor Tyrosine KinasesFlow CytometryGastrinsGene Expression Regulation, NeoplasticHumansHydrogen-Ion ConcentrationImmunohistochemistryMiceNeoplasms, ExperimentalReceptor, Cholecystokinin BReverse Transcriptase Polymerase Chain ReactionSignal TransductionStomach NeoplasmsAntineoplastic AgentsERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesGastrinsReceptor, Cholecystokinin BTrastuzumabGastric cancer (GC)GastrinGastrin/cholecystokinin B receptor (CCKBR)HER2Trastuzumab

Identifiers

PMID26173505
OpenAlexW2254987125

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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.