| 2015 |
Manic Fringe (Mfng) promotes claudin-low breast cancer through RBPJκ-dependent Notch signaling that directly induces PIK3CG transcription; PIK3CG was identified as a direct transcriptional target of Mfng-facilitated Notch signaling, and pharmacologic inhibition of PI3Kγ blocked migration and tumorsphere formation in CLBC cell lines. |
Mfng silencing/deletion in CLBC cell lines and mouse mammary tumor model, pharmacologic PI3Kγ inhibition, reporter/transcriptional target identification |
Cancer research |
Medium |
25808869
|
| 2023 |
PIK3CG activates the NLRP3 inflammasome, thereby promoting GSDMD-mediated pyroptosis in septic myocardial injury; PIK3CG siRNA suppressed NLRP3, GSDMD, IL-1β, Caspase-1, and IL-18, while PIK3CG overexpression worsened these changes, and the PIK3CG inhibitor AS-604850 reversed CLP-induced pyroptosis. |
siRNA knockdown and overexpression in HL-1 cardiomyocytes, CLP mouse model, pharmacologic inhibition (AS-604850), transcriptome analysis, Western blot |
Inflammation |
Medium |
37676465
|
| 2025 |
PIK3CG acts upstream of NLRP3 in the thalamus to mediate central post-stroke pain; PIK3CG overexpression increased NLRP3 and negated analgesic effects, while PIK3CG knockdown alleviated pain and reduced NLRP3. Simultaneous NLRP3 overexpression attenuated the analgesic effects of PIK3CG knockdown, confirming NLRP3 is downstream of PIK3CG in this pathway. Molecular docking showed Danshenol B binds PIK3CG (−9.127 kcal/mol). |
PIK3CG overexpression and knockdown in CPSP mouse model, epistasis via simultaneous NLRP3 overexpression, RNA sequencing, molecular docking |
Journal of translational medicine |
Medium |
40551174
|
| 2026 |
PIK3CG deficiency suppresses mTORC1, leading to enhanced phosphorylation of S6K2, which disrupts the nuclear S6K2 (Glu163)–p53 (Arg273) interaction and inhibits GLS2 transcription; this blocks glutamine catabolism, restricts TCA cycle entry, and causes mitochondrial ROS accumulation with suppressed pyroptosis. GLS2 overexpression rescued all phenotypes induced by PIK3CG knockdown. |
PIK3CG knockdown in vitro and in vivo, GLS2 overexpression rescue, mTORC1 pathway analysis, mitochondrial ROS and membrane potential assays, pyroptosis assays |
International immunopharmacology |
Medium |
41539001
|
| 2024 |
PIK3CG overexpression in lung cancer cells promotes migration and metastasis through enhanced MMP expression and neutrophil recruitment/activation; knockdown or pharmacologic inhibition (Eganelisib, CAY10505) reduced cell migration and MMP levels, while overexpression increased them. Co-culture with neutrophils and cathepsin G promoted lung cancer cell migration downstream of PIK3CG. |
PIK3CG knockdown and overexpression in A549 and H1299 cell lines, pharmacologic inhibition, tail-vein LLC mouse metastasis model, Transwell co-culture with neutrophils |
Biochemical genetics |
Medium |
38602596
|
| 2024 |
PIK3CG knockdown in OGD/R-injured neuronal cells inhibits autophagy by opposing AMPK/mTOR pathway activation (suppressing AMPK phosphorylation increase and restoring mTOR phosphorylation), reducing Beclin1 and LC3 II levels, decreasing apoptosis, and protecting cell proliferation. |
siRNA knockdown in SH-SY5Y cells under OGD/R, AMPK activator (metformin) co-treatment, CCK8 proliferation assay, flow cytometry apoptosis, Western blot for autophagy markers |
Neuroscience |
Low |
39603405
|
| 2023 |
PIK3CG regulates multiple myeloma cell growth via the c-Myc pathway; pharmacologic inhibition of PIK3CG (AS-605240) suppressed c-Myc expression, reduced proliferation and migration, promoted apoptosis, decreased Bcl-2/Bax ratio, and reduced vimentin expression. |
Pharmacologic inhibition with AS-605240 in MM cell lines, Western blot for c-Myc and apoptosis markers, proliferation and migration assays |
Heliyon |
Low |
38163179
|
| 2002 |
PIK3CG promoter CpG hypermethylation silences PIK3CG expression in colon cancer cells; treatment with the demethylating agent 5-aza-2'-deoxycytidine restored PIK3CG expression in DLD-1 and LoVo cells. PIK3CG encodes the catalytic subunit p110γ of PI3K, and its loss is associated with suppression of the PI3K-Akt/PKB signaling axis. |
Methylation-sensitive PCR (HpaII/MspI digestion), 5-aza-2'-deoxycytidine demethylation treatment, RT-PCR, Western blot, immunohistochemistry |
Clinical cancer research |
Medium |
12473596
|
| 2020 |
In a Trp53-deletion/Kras-activation mouse model of metastatic prostate cancer, Pik3cg is highly expressed in poorly differentiated, AR-negative tumors; pharmacologic inhibition of Pi3kγ blocked tumor cell growth in vitro, reversed epithelial-mesenchymal transition, and abated tumor metastasis in vivo. |
Genetically engineered mouse model (Trp53 KO + Kras activation), pharmacologic PI3Kγ inhibition, in vitro growth assays, in vivo metastasis assessment, immunohistochemistry |
The American journal of pathology |
Medium |
32805234
|