ArticleJournal of microbiology (Seoul, Korea)2025
Arctic lichen Cladonia borealis-induced cell death is mediated by p53-independent activation of Caspase-9 and PARP-1 signaling in human colorectal cancer cell lines.
Article in Journal of microbiology (Seoul, Korea), 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
Abstract
The anti-cancer effects of Cladonia borealis (an Arctic lichen) methanol extract (CBME) on human colon carcinoma HCT116 cells were investigated for the first time. The proliferation of the HCT116 cells treated with CBME significantly decreased in a dose- and time-dependent manner. Flow cytometry results indicated that treatment with CBME resulted in significant apoptosis in the HCT116 cells. Furthermore, immunoblotting and qRT-PCR results revealed the expression of apoptosis-related marker genes and indicated a significant downregulation of the apoptosis regulator B-cell lymphoma expression and upregulation of the cleaved form of poly (ADP-ribose) polymerase as DNA repair and apoptosis regulators and central tumor suppressor p53. Therefore, CBME significantly inhibited cell proliferation by inducing apoptosis via the mitochondrial apoptotic pathway in colon carcinoma cells. Collectively, these data suggested that CBME contained one or more compounds with anti-cancer effects and could be a potential therapeutic agent. Further studies are required to identify candidate compounds and understand the mechanism of action of CBME.
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.