ArticleRSC advances2018
TAK1 inhibition by natural cyclopeptide RA-V promotes apoptosis and inhibits protective autophagy in Kras-dependent non-small-cell lung carcinoma cells.
Article in RSC advances, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed, 11 citations in OpenAlex.
- Anticancer Ribosomally Synthesized and Post-Translationally Modified Peptides from Plants: Structures, Therapeutic Potential, and Future Directions.Current issues in molecular biology · 2024Review
- Canonical and Non-canonical TGFβ Signaling Activate Autophagy in an ULK1-Dependent Manner.Frontiers in cell and developmental biology · 2021Article
- Redox Dual-Responsive and OTheranostics · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TAK1 kinase is required for the survival of Kras-dependent non-small-cell lung carcinoma (NSCLC) cells. Here, we report that the inhibition of TAK1 by a small natural cyclopeptide (RA-V) can promote apoptosis and inhibit protective autophagy in Kras-dependent NSCLC cells. Using short hairpin RNAs to deplete K-Ras, we identified H441 and H358 cells as Kras-dependent NSCLC cells which require protective basal autophagy for cell viability. We found that RA-V could selectively kill and induce apoptosis in H441 and H358 cells but had little effect on A549 and H460 (Kras-independent) cells. Furthermore, RA-V could inhibit basal autophagy in H441 and H358 cells. Mechanistic studies further showed that RA-V inhibits the level of TAK1 phosphorylation by binding directly to TAK1, resulting in the inhibition of the autophagy-related TAK1-AMPK-mTOR pathway. In addition, we found that RA-V could inhibit TAK1-P70S6K interaction, which may also inhibit basal autophagy. Our study shows that RA-V acts as an inducer of apoptosis and inhibitor of autophagy
Identifiers
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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.