ArticleCell chemical biology2022
Mechanistic insights into cancer drug resistance through optogenetic PI3K signaling hyperactivation.
Article in Cell chemical biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 10 citations in OpenAlex.
- Recent advances of dual PROTACs for potential therapeutic applications.Molecular diversity · 2026Review
- Illuminating cancer therapy: The translational path of optogenetics.Bioactive materials · 2026Review
- An optogenetic toolkit for robust activation of FGF, BMP, & Nodal signaling in zebrafish.Developmental biology · 2026Article
- Protocol for optogenetic stimulation of cells under physical confinement.STAR protocols · 2026Article
- Approaches to visualize, quantify, and manipulate phosphoinositides in cells.Histochemistry and cell biology · 2026Review
- Oncogenic Alterations in PI3K Signaling Emulated Optogenetically Recapitulate Some Phenotypic Changes in Mammary Epithelia.ACS synthetic biology · 2026Article
- Optogenetics for Investigating and Targeting Hallmark Traits of Cancer.Biomolecules · 2026Review
- The complex interplay between diabetes mellitus and pancreatic carcinogenesis: deciphering multifactorial mechanisms and identifying emerging therapeutic vulnerabilities.Cell & bioscience · 2025Review
- Two Decades of Optogenetic Tools: A Retrospective and a Look Ahead.Advanced genetics (Hoboken, N.J.) · 2025Review
- Emerging Approaches for Studying Lipid Dynamics, Metabolism, and Interactions in Cells.Annual review of biochemistry · 2025Review
- STK32C as a Therapeutic Target in Colorectal Cancer via HSP90-PI3K/AKT/mTOR Signaling.International journal of biological sciences · 2025Article
- A "light" touch on PI3K to interrogate cancer drug resistance.Cell chemical biology · 2022Article
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperactivation of phosphatidylinositol 3-kinase (PI3K) signaling is a prominent feature in cancer cells. However, the mechanism underlying malignant behaviors in the state remains unknown. Here, we describe a mechanism of cancer drug resistance through the protein synthesis pathway, downstream of PI3K signaling. An optogenetic tool (named PPAP2) controlling PI3K signaling was developed. Melanoma cells stably expressing PPAP2 (A375-PPAP2) acquired resistance to a cancer drug in the hyperactivation state. Proteome analyses revealed that expression of the antiapoptotic factor tumor necrosis factor alpha-induced protein 8 (TNFAIP8) was upregulated. TNFAIP8 upregulation was mediated by protein translation from preexisting mRNA. These results suggest that cancer cells escape death via upregulation of TNFAIP8 expression from preexisting mRNA even though alkylating cancer drugs damage DNA.
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