ArticleMedicine2026
MAP30, a type Ⅰ ribosome-inactivating protein, inhibits hepatocellular carcinoma by inducing apoptosis through mitochondria.
Article in Medicine, 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
7 authors.
Funding
Abstract
backgroundWe have purified Momordica anti-HIV protein of 30 kDa (MAP30), a type I ribosome-inactivating protein from Momordica charantia L. with approximately 30 kDa, which inhibited protein synthesis through N-glycosylase activity and exhibited antiviral, antibacterial, antitumor and other biological activities. It is speculated that MAP30 may be a potential natural active agent for prevention and treatment of liver cancer. However, its effect on liver cancer and underlying mechanism are still unclear now. Therefore, the purpose of this manuscript was to explore the molecular mechanism of MAP30 on liver cancer.
methodsThe cell counting kit-8 assay was used to detect the proliferation of SK-Hep-1 cells. The apoptosis, cell cycle, reactive oxygen species level and mitochondrial membrane potential of SK-Hep-1 cells were detected by flow cytometry. Protein levels were determined by Western blot.
resultsIt was confirmed that MAP30 can significantly inhibit the proliferation of SK-Hep-1 cells, arrest the cell cycle in G1 phase and induce apoptosis. Further studies on apoptosis-related proteins showed that the expression of caspase-3, caspase-9, poly (ADP-ribose) polymerase and B-cell lymphoma 2 proteins decreased synchronously in a time- and dose-dependent manner. In addition, MAP30-induced apoptosis of SK-Hep-1 cells was found to be closely related to the mitochondrial pathway through the increase of reactive oxygen species and the decrease of mitochondrial membrane potential.
conclusionThe manuscript indicated that MAP30 may be a potential antitumor drug which provided an experimental basis for further exploration of the mechanism of MAP30 prevention and treatment of liver cancer, and was expected to be applied in medicine and biotechnology.
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.