ArticleSmall GTPases2023
PI3K Functions Downstream of Cdc42 to Drive Cancer phenotypes in a Melanoma Cell Line.
Article in Small GTPases, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06924697 (Effect of Glucagon-like Peptide-1), which is not on this map. Cited by 4 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.
Effect of Glucagon-like Peptide-1 (GLP-1) Receptor Agonist Stimulation on Smoking Consumption in Type 2 Diabetes Patients: Study Protocol of a Randomized, Parallel -Controlled Clinical Trial
Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Rho GTPases in cancer resistance: mechanisms, vulnerabilities, and therapeutic opportunities.Biochemical Society transactions · 2026Review
- Tetracenomycin Aglycones Primarily Inhibit Cell Growth and Proliferation in Mammalian Cancer Cell Lines.Applied sciences (Basel, Switzerland) · 2025Article
- CDC42 supports HBV entry by NTCP translocation to the plasma membrane and macropinocytosis.EMBO reports · 2025Article
- Impact of Physical Exercise on Melanoma Hallmarks: Current Status of Preclinical and Clinical Research.Journal of Cancer · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rho proteins are part of the Ras superfamily, which function to modulate cytoskeletal dynamics including cell adhesion and motility. Recently, an activating mutation in Cdc42, a Rho family GTPase, was found in a patient sample of melanoma. Previously, our work had shown the PI3K was important downstream of mutationally active Cdc42. Our present study sought to determine whether PI3K was a crucial downstream partner for Cdc42 in a melanoma cells line with a BRAF mutation, which is the most common mutation in cutaneous melanoma. In this work we were able to show that Cdc42 contributes to proliferation, anchorage-independent growth, cell motility and invasion. Treatment with a pan-PI3K inhibitor was able to effectively ameliorate all these cancer phenotypes. These data suggest that PI3K may be an important target downstream of Cdc42 in melanoma.
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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.