ArticleOncotarget2014
Dual Aurora A and JAK2 kinase blockade effectively suppresses malignant transformation.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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
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.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Structure-guided discovery of a dual JAK2/RAGE modulator reveals a computationally driven strategy for targeting convergent oncogenic signaling in renal cell carcinoma.Journal of computer-aided molecular design · 2026Article
- Molecular targets and therapeutics in chemoresistance of triple-negative breast cancer.Medical oncology (Northwood, London, England) · 2021Review
- JAK/STAT inhibition in macrophages promotes therapeutic resistance by inducing expression of protumorigenic factors.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- The role of aurora A and polo-like kinases in high-risk lymphomas.Blood advances · 2019Review
- Inhibition of AURKA kinase activity suppresses collective invasion in a microfluidic cell culture platform.Scientific reports · 2017Article
- Targeting Aurora kinase A and JAK2 prevents GVHD while maintaining Treg and antitumor CTL function.Science translational medicine · 2017Article
- Alisertib demonstrates significant antitumor activity in bevacizumab resistant, patient derived orthotopic models of glioblastoma.Journal of neuro-oncology · 2017Article
- Search for Potent and Selective Aurora A Inhibitors Based on General Ser/Thr Kinase Pharmacophore Model.Pharmaceuticals (Basel, Switzerland) · 2016Article
- Co-expression of mitosis-regulating genes contributes to malignant progression and prognosis in oligodendrogliomas.Oncotarget · 2015Article
- Development of novel ACK1/TNK2 inhibitors using a fragment-based approach.Journal of medicinal chemistry · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Aurora A and JAK2 kinases are involved in cell division and tumor cell survival, respectively. Here we demonstrate that ectopic expression of Aurora A and JAK2 together is more effective than each alone at inducing non-transformed cells to grow in an anchorage-independent manner and to invade. Furthermore, siRNA silencing or pharmacological inhibition of Aurora A and JAK2 with Alisertib and Ruxolitinib, respectively, is more effective than blocking each kinase alone at suppressing anchorage-dependent and -independent growth and invasion as well as at inducing apoptosis. Importantly, we have developed dual Aurora and JAK inhibitors, AJI-214 and AJI-100, which potently inhibit Aurora A, Aurora B and JAK2 in vitro. In human cancer cells, these dual inhibitors block the auto-phosphorylation of Aurora A (Thr-288) and the phosphorylation of the Aurora B substrate histone H3 (Ser-10) and the JAK2 substrate STAT3 (Tyr-705). Furthermore, AJI-214 and AJI-100 inhibit anchorage dependent and independent cell growth and invasion and induce G2/M cell cycle accumulation and apoptosis. Finally, AJI-100 caused regression of human tumor xenografts in mice. Taken together, our genetic and pharmacological studies indicate that targeting Aurora A and JAK2 together is a more effective approach than each kinase alone at inhibiting malignant transformation and warrant further advanced pre clinical investigations of dual Aurora A/JAK2 inhibitors as potential anti tumor agents.
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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.