ArticleApoptosis : an international journal on programmed cell death2026
Heteronemin suppresses chemoresistant oral squamous cell carcinoma cells through ROS-mediated apoptosis and cuproptosis-associated mitochondrial stress.
Article in Apoptosis : an international journal on programmed cell death, 2026. 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemoresistance remains a major barrier in treating oral squamous cell carcinoma (OSCC). This study investigated whether the marine-derived sesterterpenoid heteronemin (HET) suppresses chemoresistant OSCC (SAS-CR) cells and elucidated its underlying mechanisms. HET dose- and time-dependently reduced SAS-CR viability, inhibited clonogenic growth, and exhibited stronger cytotoxicity than cisplatin or 5-fluorouracil. Furthermore, HET induced S-phase arrest by downregulating proliferation and cell-cycle proteins (PCNA, c-Myc, cyclin A, cyclin D3, CDK4, and CDK6). Concurrently, it triggered intrinsic apoptosis, characterized by mitochondrial depolarization, upregulated cleaved caspase-3/PARP and Bax, and downregulated Bcl-2. This caspase-dependent apoptosis was partially reversed by pan-caspase inhibitor Z-VAD-FMK. Transcriptomic profiling linked these phenotypes to metabolic stress, revealing alterations in the tricarboxylic acid cycle, mitochondrial respiration, and copper homeostasis. Consistently, HET elevated intracellular Cu
Indexed as
Identifiers
42315805What 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.