ArticleTechnology in cancer research & treatment
Potential Molecular Mechanisms of AURKB in the Oncogenesis and Progression of Osteosarcoma Cells: A Label-Free Quantitative Proteomics Analysis.
Article in Technology in cancer research & treatment. 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 It has been retracted, and should not be counted.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 6 papers.
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
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
6 citing papers in PubMed, 15 citations in OpenAlex.
- Aurora-B: a novel biomarker in the invasion and metastasis of osteosarcoma.Biomarkers in medicine · 2024Review
- 8a, a New Acridine Antiproliferative and Pro-Apoptotic Agent Targeting HDAC1/DNMT1.International journal of molecular sciences · 2021Article
- Mitotic kinases as drivers of the epithelial-to-mesenchymal transition and as therapeutic targets against breast cancers.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- The Identification of Key Gene Expression Signature and Biological Pathways in Metastatic Renal Cell Carcinoma.Journal of Cancer · 2020Article
- Article
- CENPE, PRC1, TTK, and PLK4 May Play Crucial Roles in the Osteosarcoma Progression.Technology in cancer research & treatmentArticle
Corrections and comments
- Retraction · 2025-03-25Concerns/Issues about Image · Duplication of/in Image · Error in Image · Euphemisms for Duplication · Investigation by Journal/Publisher · Objections by Author(s) · Original Data and/or Images not Provided and/or not Available · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous study indicated that knockdown of Aurora-B inhibit the proliferation of osteosarcoma cells. But the function and molecular mechanisms of Aurora-B in osteosarcoma cells growth and metastasis remains unclear. The aim of this study was to investigate the molecular mechanisms of Aurora-B in the progression of osteosarcoma. Osteosarcoma cells (U2-OS and 143B) were treated with specific Lentivirus-Vectors (up or downregulation Aurora-B). The ability of cells proliferation, migration, and invasion was measured using Cell-Counting Kit-8, wound healing and transwell invasion assays. Furthermore, based on label-free quantitative proteomic analysis of potential molecular mechanisms of Aurora-B in human 143B cells. A total of 25 downregulated and 76 upregulated differentially expressed proteins were screened in terms of the change in their expression abundance. We performed functional annotation and functional enrichment analyses. Gene ontology enrichment, KEGG analysis, and protein-protein interaction networks were constructed and analyzed. We found that the PTK2 may play an important role in the progression of osteosarcoma cells. Finally, Western blot revealed that expression of PTK2, AKT, PI3K, and nuclear factor-kappaB increased after over expression of Aurora-B. Overall, these data highlight that Aurora-B may promote the malignant phenotype of osteosarcoma cells by activating the PTK2/PI3K/AKt/nuclear factor-KappaB pathway.
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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.