Evidence map›Paper›PMID 24947165›Full record

ArticleWorld journal of surgical oncology2014

Anti-apoptotic effects of osteopontin through the up-regulation of Mcl-1 in gastrointestinal stromal tumors.

Kai-Hsi Hsu, Hung-Wen Tsai, Pin-Wen Lin, Yun-Shang Hsu, Pei-Jung Lu, Yan-Shen Shan

Open access · goldAbstract read
In one paragraph

Article in World journal of surgical oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. NEK2 drives pathogenesis, drug resistance, and LMP1 expression in EBV-positive non-Hodgkin lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Ameliorating Effect of Osteopontin on HCellular and molecular neurobiology · 2018
    Article
  6. Article
  7. Review
  8. Osteopontin splice variants expression is involved on docetaxel resistance in PC3 prostate cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    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

6 authors at 2 institutions in 1 country.

Kai-Hsi Hsu
Hung-Wen Tsai
Pin-Wen Lin
Yun-Shang Hsu
Pei-Jung Lu
Yan-Shen ShanDepartment of Surgery, National Cheng Kung University, College of Medicine, Tainan 70428, Taiwan. ysshan@mail.ncku.edu.tw.
National Cheng Kung University · TWSouthern Taiwan University of Science and Technology · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOsteopontin (OPN) is a secreted phosphoprotein expressed by neoplastic cells involved in the malignant potential and aggressive phenotypes of human malignancies, including gastrointestinal stromal tumors (GISTs). Our previous study showed that OPN can promote tumor cell proliferation in GISTs. In this series, we further aim to investigate the effect of OPN on apoptosis in GISTs.

methodsThe expression of apoptotic and anti-apoptotic proteins in response to OPN was evaluated. In vitro effects of OPN against apoptosis in GIST were also assessed. GIST specimens were also used for analyzing protein expression of specific apoptosis-related molecules and their clinicopathologic significance.

resultsUp-regulation of β-catenin and anti-apoptotic proteins Mcl-1 with concomitant suppression of apoptotic proteins in response to OPN was noted. A significant anti-apoptotic effect of OPN on imatinib-induced apoptosis was identified. Furthermore, Mcl-1 overexpression was significantly associated with OPN and β-catenin expression in tumor tissues, as well as worse survival clinically.

conclusionsOur study identifies anti-apoptotic effects of OPN that, through β-catenin-mediated Mcl-1 up-regulation, significantly antagonized imatinib-induced apoptosis in GISTs. These results provide a potential rationale for therapeutic strategies targeting both OPN and Mcl-1 of the same anti-apoptotic signaling pathway, which may account for resistance to imatinib in GISTs.

Indexed as

ApoptosisDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticAntineoplastic AgentsBenzamidesbeta CateninBlotting, WesternCell ProliferationFemaleGastrointestinal Stromal TumorsHumansImatinib MesylateImmunoenzyme TechniquesMaleMiddle AgedMyeloid Cell Leukemia Sequence 1 ProteinAntineoplastic AgentsBenzamidesbeta CateninImatinib MesylateMCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinOsteopontinPiperazinesPyrimidines

Identifiers

PMID24947165
PMCPMC4080696
OpenAlexW2158889091

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.