ArticleJournal of carcinogenesis2009
MET/PKCbeta expression correlate with metastasis and inhibition is synergistic in lung cancer.
Article in Journal of carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- Enzastaurin inhibits invasion and metastasis in lung cancer by diverse molecules.British journal of cancer · 2010Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundTreatment of non-small cell lung cancer (NSCLC) remains a difficult task in oncology. Targeted inhibition of oncogenic proteins is promising. In this study, we evaluate the expression of MET and PKCbeta and in vitro effects of their inhibition using SU11274 and enzastaurin (LY317615.HCl) respectively. MATERIALS AND
methodsPatient samples were analyzed by immunohistochemistry for expression of PKCbeta and MET, utilizing tissue microarrays under an IRB-approved protocol. Expression of PKCbeta and MET was evaluated in cell lines by immunoblotting. Treatment with SU1174 against MET and enzastaurin against PKCbeta was performed in H1993 and H358 cell lines, and cell proliferation and downstream signaling (phosphorylation of MET, AKT, FAK, and GSK3beta) were evaluated by immunoblotting. Statistical analysis was performed using SPSS 16.0.
resultsExpression of MET positively correlated with lymph node metastases (p=.0004), whereas PKCbeta showed no correlation (p=0.204). MET and PKCbeta expression were also strongly correlated (p<0.001). Expression of MET was observed in 5/8 cell lines (H358, H1703, A549, H1993, H2170; absent from H522, H661, or SW1573), whereas PKCbeta expression was observed in 8/8 cell lines. Cell proliferation was significantly impaired by treatment with SU11274 and enzastaurin, and their effects were synergistic in combination (CI=0.32 and 0.09). Phosphorylation of MET, FAK, AKT, and GSK3beta were strongly inhibited with both agents in combination.
conclusionsConcomitant inhibition of MET and PKCbeta significantly increased cytotoxicity in vitro against NSCLC, disrupting important downstream signaling pathways. Further evaluation in animal models is warranted.
Identifiers
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Registered trials
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.