ArticleIET systems biology
Decoding the Anti-Tumour Mechanism of ɑ-Solanine: SRC Inhibition and Ferroptosis Induction in Colon Cancer.
Article in IET systems biology. 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
4 authors.
Funding
Abstract
α-Solanine, a steroidal alkaloid glycoside, exhibits significant anti-tumour properties with potential therapeutic applications in colon cancer. Its relevance was explored through network pharmacology, bioinformatics analysis and experimental validation. α-Solanine treatment significantly inhibited HT29 colon cancer cell proliferation and migration dose-dependently, reducing Ki67 and PCNA expression markers. Target prediction using PharmMapper and GeneCards databases revealed 90 potential targets, with network analysis identifying SRC as the key molecular target. Molecular docking confirmed stable α-solanine-SRC binding (-9.3 kcal/mol). TCGA analysis demonstrated SRC upregulation in colon cancer across tumour stages T1-T4, with high expression correlating negatively with immune infiltration and poor prognosis. Pathway analysis revealed SRC's involvement in PI3K/AKT/mTOR signalling, regulating ferroptosis-related genes. Experimental validation showed α-solanine increased ROS, MDA and iron levels while decreasing GSH, promoting ferroptosis. Gene silencing confirmed SRC's critical role in cancer progression, with α-solanine's effects suppressed upon SRC upregulation. These findings suggest that SRC is a potential target of α-solanine, and that its anticancer effects may involve inhibition of SRC and suppression of the PI3K/AKT/mTOR pathway. The ferroptosis-mediated mechanisms highlight α-solanine's therapeutic potential and suggest promising avenues for colon cancer treatment development.
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.