ArticleInternational journal of clinical and experimental pathology2017
Capn4 induces human renal cancer cell proliferation by activating NF-κB signaling pathway through FAK phosphorylation.
Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Calpain Small Subunit 1 Protein in the Prognosis of Cancer Survivors and Its Clinicopathological Correlation.BioMed research international · 2019Pooled it
- MiRNA-124 regulates the sensitivity of renal cancer cells to cisplatin-induced necroptosis by targeting the CAPN4-CNOT3 axis.Translational andrology and urology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous study found that higher Capn4 mRNA level is observed in patients with more advanced pathological stage of ccRCC and is also associated with decreased overall survival of patients with ccRCC. However, the mechanism by which Capn4 promotes progression of RCC is not understood. In the present study, we found that over-expression of Capn4 in RCC cells enhances tumor cell growth and down-regulation of Capn4 in RCC cells decreases tumor cell growth in vitro. Interestingly, Capn4 was found to increase phosphorylation of specific tyrosine residues of FAK and subsequent activate NF-κB p65 phosphorylation. Furthermore, Capn4-mediated cell proliferation of RCC cells required up-regulation of NF-κB p65 phosphorylation through activation of FAK signaling pathway. Taken together, our data showed that Capn4 can contribute to RCC growth via activation of the FAK and the downstream signaling pathways leading to the activation of NF-κB.
Indexed as
Identifiers
31966590PMC6965247What 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.