Phosphatidylinositol 3-kinase 92E Dmel_CG4141
Phosphatidylinositol 3-kinase 92E Dmel_CG4141
Overview
Phosphatidylinositol 3-kinase 92E Dmel_CG4141 is a Drosophila melanogaster phosphoinositide 3-kinase (PI3K) pathway component associated with the broader PI3K signaling network. In biomedical literature, PI3K enzymes are central regulators of cell growth, survival, metabolism, and immune signaling through downstream activation of AKT and mechanistic target of rapamycin kinase (mTOR). Because of this, PI3K-related pathways are frequently studied in cancer, metabolic disease, vascular abnormalities, and immune regulation.
Although the entity name reflects a Drosophila gene annotation, the recent research contexts provided focus on the conserved PI3K signaling axis in human and mouse disease models. Across these studies, PI3K is discussed as part of oncogenic and metabolic signaling cascades, often in combination with AKT, mTOR, STAT3, c-ABL, LCK, FOXO1, and related regulators. This makes the pathway biologically significant both as a mechanistic node and as a therapeutic target in diseases such as venous malformations, non-small cell lung cancer, breast cancer, lymphoma, liver metastasis, and type 2 diabetes.
Recent Publications Focus
Below is a summary of the newest research publications targeting Phosphatidylinositol 3-kinase 92E Dmel_CG4141 (sorted by publication date).
PMID: 42090479 — Polymeric rapamycin nanoparticles encapsulating ponatinib cause regression of venous malformations in mice.
This study linked venous malformations to activation of the PI3K/AKT/mTOR pathway together with c-ABL signaling. The work evaluated polymeric rapamycin nanoparticles encapsulating ponatinib, using a 30-nanometer nanoparticle formulation to deliver the agents in mice. The reported conclusion was that this combined approach caused regression of venous malformations, supporting the therapeutic relevance of suppressing PI3K pathway signaling in this vascular disease context.PMID: 42062032 — Nobiletin inhibits non-small cell lung cancer through TRKC and exhibits a synergistic effect with the HDAC inhibitor.
In A-549 cells, transcriptome sequencing indicated that combination treatment primarily inhibited tumor cell proliferation by modulating TRKC protein expression and suppressing phosphorylation of the PI3K/AKT/mTOR signaling pathway. The study therefore positioned PI3K signaling as part of the downstream mechanism associated with the anti-proliferative effect of nobiletin and its synergy with an HDAC inhibitor.PMID: 42035271 — Design, Synthesis, and Biological Evaluation of Novel Triazine-Based Dual Histone Deacetylase/phosphatidylinositol 3-kinase Inhibitors for breast cancer Therapy.
This publication focused on the design, synthesis, and biological evaluation of triazine-based multitarget inhibitors intended to simultaneously inhibit HDAC and PI3K signaling in breast cancer, including MDA-MB-231 cells. The rationale was based on the observation that dysregulation of the PI3K/AKT/mTOR and HDAC pathways contributes to triple-negative breast cancer progression and therapeutic resistance. Molecular docking and dynamics simulations were used to support the proposed binding behavior of the compounds, and the study framed dual targeting as a strategy to improve breast cancer therapy.PMID: 41963620 — Hepatocyte-derived LRG1 primes the liver for metastasis and impairs immunotherapy.
This study reported that hepatic LRG1 induced by tumor-associated inflammation via IL-6/STAT3 signaling promotes liver metastasis through formation of a TGFBR/PI3K/AKT axis-driven neutrophil extracellular trap program. The findings connected PI3K signaling to metastatic niche formation and impaired immunotherapy response, highlighting its role in tumor microenvironment remodeling and metastatic progression.PMID: 41964005 — B7-H3 (CD276) in exosome biogenesis and the tumor microenvironment: a new therapeutic nexus.
The publication described B7-H3/CD276 as a regulator that activates pathways including STAT3, PI3K, and lipid metabolism, thereby amplifying oncogenic signaling and promoting a pro-tumor tumor microenvironment. In this context, PI3K was presented as part of a broader signaling network linked to exosome biology and immune-modulatory cancer phenotypes.PMID: 41946709 — Ponatinib inhibits LCK and PI3K signaling and promotes CD8+ T stem cell memory cell development.
This study showed that ponatinib inhibits LCK and PI3K signaling to enhance the transcriptional functions of TCF7 and FOXO1, thereby promoting CD8+ T stem cell memory cell differentiation. The work extended PI3K biology into T-cell fate regulation and suggested that pathway inhibition can support beneficial immune-memory phenotypes.PMID: 41940860 — Effects of Psyllium Husk on Metabolic Regulators, insulin resistance, and SIRT6 in Liver and Muscle of Type 2 Diabetic Rats.
In a type 2 diabetes rat model, the study discussed PI3K among biomarkers relevant to glucose homeostasis and metabolic regulation, alongside GLUT4, SIRT6, nesfatin-1, GLP-1, leptin, and IGF1. Although the publication context provided here does not specify a direct PI3K-targeted intervention, it places PI3K within the network of insulin resistance and metabolic control in liver and muscle.PMID: 41736531 — Targeting signaling pathways in lymphoma: From molecular mechanisms to clinical breakthroughs.
This review dissected key oncogenic survival networks, including the B-cell receptor, PI3K/AKT/mTOR, JAK/STAT, and B-cell lymphoma 2 apoptosis pathways. In the lymphoma setting, PI3K was presented as a foundational signaling axis with established clinical relevance and ongoing therapeutic interest, consistent with broader efforts to target pathway dependencies in hematologic malignancy.
Background PMIDs
- [PMID 42090479]
- [PMID 41963620]
Target PMIDs
- [PMID 41940860]
- [PMID 42062032]
- [PMID 42035271]
- [PMID 41964005]
- [PMID 41946709]
- [PMID 41736531]