ArticleMolecular biology reports2020
Wnt/PCP signalling cascade disruption by JNK inhibition as a potential mechanism underlying the teratogenic effects of potato glycoalkaloids.
Article in Molecular biology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Glycoalkaloids Affect the Animal Nervous System: A Review.Journal of toxicology · 2026Review
- Fundamental origins of neural tube defects with a basis in genetics and nutrition.Experimental brain research · 2025Review
- The Therapeutic Value of Solanum Steroidal (Glyco)Alkaloids: A 10-Year Comprehensive Review.Molecules (Basel, Switzerland) · 2023Review
- Wnt signaling in colorectal cancer: pathogenic role and therapeutic target.Molecular cancer · 2022Review
- Anticancer activity of glycoalkaloids fromFrontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is hypothesised that the inhibition of the non-canonical Wnt/PCP intracellular signalling cascade by potato glycoalkaloids, [Formula: see text]-solanine and [Formula: see text]-chaconine, results in an increased risk of neural tube defects (NTDs). One very prominent intracellular signalling pathway with substantial implications in the development and closure of the neural tube is the Wnt/PCP pathway. Experimental inhibition of this results in NTDs. A vital element of this signalling cascade is JNK, which controls the transcription of DNA, which controls cell polarity and directional cell migration. JNK inhibition also results in NTDs experimentally. Through their use in cancer research, [Formula: see text]-solanine and [Formula: see text]-chaconine were found to inhibit metastasis by inhibiting JNK, among other intracellular signalling molecules. Thus, this shows that potato glycoalkaloids increase the likelihood of causing NTDs by inhibiting the proper functioning of JNK in the Wnt/PCP pathway, resulting in defective neural tube closure.
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Registered trials
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