ArticleAmerican journal of cancer research2025
Cynaropicrin induces the apoptosis of colorectal cancer cells by elevating reactive oxygen species and activating the JNK/p38 MAPK.
Article in American journal of cancer research, 2025. 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of new therapeutics for colorectal cancer (CRC) is urgently needed to address the limitations of current treatments. This study was performed to investigate the anticancer activity of cynaropicrin (a natural product) in CRC HCT116 cells and an oxaliplatin (Ox)-resistant HCT116 strain (HCT116-OxR). MTT cell viability assays showed that cynaropicrin inhibited the growth of HCT116 and HCT116-OxR cells in a dose- and time-dependent manner. Cynaropicrin also induced apoptosis, as identified by an Annexin V-FITC/PI double staining, and this apoptosis was accompanied by the phosphorylations of JNK and p38 MAPK. In addition, treatment with the kinase-specific inhibitors SP600125 and SB203580 confirmed that this apoptosis was mediated by JNK and p38 MAPK. Flow cytometry analysis using the CellROX™ kit showed cynaropicrin increased reactive oxygen species (ROS) levels, and N-acetylcysteine pretreatment confirmed ROS mediated the cytotoxicity of cynaropicrin. Flow cytometry with propidium iodide staining and western blot analysis indicated that cynaropicrin induced cell cycle arrest at the G2/M phase by modulating cell cycle regulators, and western blot analysis revealed that cynaropicrin altered the balance of Bcl-2 family proteins. Also, flow cytometry using the Muse™ Multi-Caspase Kit showed cynaropicrin activated multiple caspases, the crucial roles of which were confirmed using the pan-caspase inhibitor Z-VAD-FMK. In conclusion, cynaropicrin demonstrated anticancer activity against CRC cells by elevating ROS levels, activating JNK and p38 MAPK, and inducing cell cycle arrest leading to apoptosis. Further studies are warranted to evaluate the therapeutic potential of cynaropicrin in CRC.
Indexed as
Identifiers
What Socratic 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 Socratic graph.