ArticleCells2024
Down-Regulation of AKT Proteins Slows the Growth of Mutant-KRAS Pancreatic Tumors.
Article in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed.
- CDC6/THBS1 accelerates pancreatic cancer progression via AKT-mediated glycolytic reprogramming.Cell death & disease · 2026Article
- Loss of PIK3CA AllowsCells · 2026Article
- Loss of PIK3CA allowsbioRxiv : the preprint server for biology · 2026Article
- Selective targeting of the AKT1 (E17K) mutation: advances in precision oncology and therapeutic design.Discover oncology · 2025Article
- Harnessing the Therapeutic Potential of Pomegranate Peel-Derived Bioactive Compounds in Pancreatic Cancer: A Computational Approach.Pharmaceuticals (Basel, Switzerland) · 2025Article
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Abstract
Serine/threonine kinase AKT isoforms play a well-established role in cell metabolism and growth. Most pancreatic adenocarcinomas (PDACs) harbor activation mutations of KRAS, which activates the PI3K/AKT signaling pathway. However, AKT inhibitors are not effective in the treatment of pancreatic cancer. To better understand the role of AKT signaling in mutant-KRAS pancreatic tumors, this study utilized proteolysis-targeting chimeras (PROTACs) and CRISPR-Cas9-genome editing to investigate AKT proteins. The PROTAC down-regulation of AKT proteins markedly slowed the growth of three pancreatic tumor cell lines harboring mutant KRAS. In contrast, the inhibition of AKT kinase activity alone had very little effect on the growth of these cell lines. The concurrent genetic deletion of all AKT isoforms (AKT1, AKT2, and AKT3) in the KPC (
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