ArticleOncology letters2018
Pyk2 promotes tumor progression in renal cell carcinoma.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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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
3 citing papers in PubMed, 4 citations in OpenAlex.
- RB1CC1 functions as a tumor-suppressing gene in renal cell carcinoma via suppression of PYK2 activity and disruption of TAZ-mediated PDL1 transcription activation.Cancer immunology, immunotherapy : CII · 2021Article
- Pyk2 level is a novel prognostic marker for patients with esophageal squamous cell carcinoma after radical surgery.Virchows Archiv : an international journal of pathology · 2021Article
- MET-Pyk2 Axis Mediates Acquired Resistance to FGFR Inhibition in Cancer Cells.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proline-rich tyrosine kinase 2 (Pyk2), a member of the focal adhesion kinase family, has recently been associated with tumor development. However, the role of Pyk2 in renal cell carcinoma (RCC) remains unexplored. The present study investigated the expression pattern, clinical significance, and function of Pyk2 in RCC. By using a reverse transcription-quantitative polymerase chain reaction, tissue microarray and immunohistochemistry, it was demonstrated that RCC tissues display a higher Pyk2 expression compared with paired adjacent nontumor tissues. Furthermore, it was revealed that Pyk2 upregulation was associated with poor clinical outcomes in patients with RCC. By using loss-of-function approaches, it was demonstrated that Pyk2 knockdown reduced cell viability, invasive ability and migratory ability, and increased apoptosis in RCC cell lines. In contrast, Pyk2 overexpression promoted tumor cell proliferation, invasion and migration and reduced apoptosis. Collectively, the results of the present study present the tumor-promoting function of Pyk2 in RCC and thus provide molecular evidence for novel tyrosine kinase inhibitors as novel therapeutic options for RCC.
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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 Socratic graph.