ArticleProceedings of the National Academy of Sciences of the United States of America2023
Small-molecule targeting of GPCR-independent noncanonical G-protein signaling in cancer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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
11 citing papers in PubMed.
- Small-molecule modulation of β-arrestins.Nature · 2026Article
- Identification of a small molecule that targets activator of G-protein signaling 8.The journal of physiological sciences : JPS · 2026Article
- TRV130 inhibits colon cancer progression via suppressing the Hedgehog signaling pathway: in vitro and in vivo evidence.Hereditas · 2026Article
- The role of RGS12 in tissue repair and human diseases.Genes & diseases · 2025Review
- Discovery ofActa pharmaceutica Sinica. B · 2025Article
- Article
- Get Ready to Sharpen Your Tools: A Short Guide to Heterotrimeric G Protein Activity Biosensors.Molecular pharmacology · 2024Review
- Iridium(III) carbene complexes as potent girdin inhibitors against metastatic cancers.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Heterotrimeric G protein signaling without GPCRs: The Gα-binding-and-activating (GBA) motif.The Journal of biological chemistry · 2024Review
- Synaptic plasticity via receptor tyrosine kinase/G-protein-coupled receptor crosstalk.Cell reports · 2024Article
- The G Protein-Coupled Estrogen Receptor (GPER): A Critical Therapeutic Target for Cancer.Cells · 2023Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Activation of heterotrimeric G-proteins (Gαβγ) by G-protein-coupled receptors (GPCRs) is a quintessential mechanism of cell signaling widely targeted by clinically approved drugs. However, it has become evident that heterotrimeric G-proteins can also be activated via GPCR-independent mechanisms that remain untapped as pharmacological targets. GIV/Girdin has emerged as a prototypical non-GPCR activator of G proteins that promotes cancer metastasis. Here, we introduce IGGi-11, a first-in-class small-molecule inhibitor of noncanonical activation of heterotrimeric G-protein signaling. IGGi-11 binding to G-protein α-subunits (Gαi) specifically disrupted their engagement with GIV/Girdin, thereby blocking noncanonical G-protein signaling in tumor cells and inhibiting proinvasive traits of metastatic cancer cells. In contrast, IGGi-11 did not interfere with canonical G-protein signaling mechanisms triggered by GPCRs. By revealing that small molecules can selectively disable noncanonical mechanisms of G-protein activation dysregulated in disease, these findings warrant the exploration of therapeutic modalities in G-protein signaling that go beyond targeting GPCRs.
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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.