ArticleMolecular and clinical oncology2024
Analysis of naproxen activation of cell death pathways in Colo320 cells.
Article in Molecular and clinical oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer is a life-threatening and prevalent type of cancer. However, a number of current treatments have serious side effects, which increase the need for alternatives. Non-steroidal anti-inflammatory drugs have potential chemopreventive capabilities. The present study aimed to confirm this, as well as to investigate potential pathways and reasons for this trait. To accomplish this, cancerous Colo320 and healthy CCD-18 cells were treated with various concentrations of naproxen sodium (NS). A caspase-3 assay revealed a statistically significant increase in caspase-3 activity in Colo320 cells (300%; P<0.01), but not in CCD-18 cells. This chemical was also associated with a significant decrease in Colo320 cell survival (-72.888%; P<0.01), but not CCD-18 cell survival. Furthermore, NS was found to significantly decrease the migration of Colo320 cells (86.58%; P<0.01). Finally, RNA sequencing of cells treated with NS revealed the statistically significant downregulation of the mucin 5B, oligomeric mucus/gel-forming, S100 calcium binding protein A9 and mucin 5AC, oligomeric mucus/gel-forming genes, which are upregulated in colorectal cancer and are known to contribute to cancer proliferation, stemness and drug resistance. These novel biological pathway results were further confirmed using ELISAs. The present study identified a novel molecular mechanism of the anti-colorectal cancer activity of NS.
Indexed as
Identifiers
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.