ArticleInternational journal of cancer2012
A multiplicity of anti-invasive effects of farnesyl transferase inhibitor SCH66336 in human head and neck cancer.
Article in International journal of cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 8 papers.
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.
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.
Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Loss of CENPF leads to developmental failure in mouse embryos.Cell cycle (Georgetown, Tex.) · 2019Article
- New tricks for human farnesyltransferase inhibitor: cancer and beyond.MedChemComm · 2017Review
- Farnesyl transferase inhibitor FTI-277 inhibits breast cell invasion and migration by blocking H-Ras activation.Oncology letters · 2016Article
- Ninjurin1 inhibits colitis-mediated colon cancer development and growth by suppression of macrophage infiltration through repression of FAK signaling.Oncotarget · 2016Article
- Acquired resistance to 5-fluorouracil via HSP90/Src-mediated increase in thymidylate synthase expression in colon cancer.Oncotarget · 2015Article
- Insulin-like growth factor binding protein-3 inhibits cell adhesion via suppression of integrin β4 expression.Oncotarget · 2015Article
- MicroRNA-503 acts as a tumor suppressor in glioblastoma for multiple antitumor effects by targeting IGF-1R.Oncology reports · 2014Article
- Cyclizations of phenylethyl-substituted pyridinecarboxaldehydes.Tetrahedron · 2013Article
Corrections and comments
- Retraction · 2024-10-22Concerns/Issues about Image · Duplication of Data · Duplication of/in Image · Investigation by Journal/Publisher · Investigation by Third Party · Original Data and/or Images not Provided and/or not Available · Unreliable Data · Unreliable Results and/or Conclusions · · see also: https://pubpeer.com/publications/EC79E01D04EEB78AA5AEC0857C2544
- Retracted
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Metastasis is a critical event in the progression of head and neck squamous cell carcinoma (HNSCC) and closely correlates with clinical outcome. We previously showed that the farnesyl transferase inhibitor SCH66336 has antitumor activities in HNSCC by inducing the secretion of insulin-like growth factor binding protein 3 (IGFBP-3), which in turn inhibits tumor growth and angiogenesis. In our study, we found that SCH66336 at a sublethal dose for HNSCC inhibited the migration and invasion of HNSCC cells. The inhibitory effect of SCH66336 was associated with the blockade of the IGF-1 receptor (IGF-1R) pathway via suppressing IGF-1R itself and Akt expression. Consistent with previous work, induction of IGFBP-3 by SCH66336 also contributed in part to the anti-invasive effect. SCH66336 treatment also reduced the expression and activity of the urokinase-type plasminogen activator (uPA) and matrix metalloproteinase 2 (MMP-2), both important regulators of tumor metastasis. The effect of SCH66336 on uPA activity was inhibited partly by knockdown of IGFBP-3 using small interfering RNA. The inhibitory effect of SCH66336 on migration or invasion was attenuated partly or completely by knockdown of IGFBP-3, Akt or IGF-1R expression, respectively. Our results demonstrate that the IGF-1R pathway plays a major role in the proliferation, migration and invasion of HNSCC cells, suggesting that therapeutic obstruction of the IGF-1R pathway would be a useful approach to treating patients with HNSCC.
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What OpenQuestion holds
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.