PIK3CB (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta)

The integrated analysis of longitudinal WES data from primary tumors and matched PDXs enabled the identification of a core set of conserved, potentially deleterious mutations. The four prioritized mutations (PTPRK, PIK3CB, LRP1B, and IGF2R) provide new insights into the genetic landscape of gastric cancer and represent promising candidates for the development of targeted therapeutic strategies.

Furthermore, HERC1 overexpression enhanced the inhibition of gemcitabine on tumor growth by suppressing autophagy in vivo. In conclusion, HERC1 inhibited autophagy by inactivating PIK3CB-mediated PI3K/AKT signaling via promoting KAT2A degradation, thereby enhancing the gemcitabine sensitivity in lung cancer.

RT-qPCR revealed their stage-specific overexpression during CCSCs induction and showed their potential as therapeutic targets. The LCNP-T-M platform provides an effective technical framework and theoretical foundation for investigating CCSCs' mechanisms and target discovery.

MTT assay showed that 6 and 9b were 4.5 and 2 times more potent than doxorubicin against MCF-7 cells, while 9a and 13b were 10 and 7.5 times more effective against MDA-MB-231 cells, respectively...Compound 13b exhibited comparable EGFRL858R inhibition to lapatinib and outperformed pictilisib against PI3Kα, PI3Kβ, and PI3Kδ. Compound 6 showed greater ARO inhibition than letrozole, while being slightly less potent than pictilisib against PI3Kα and PI3Kβ...Docking studies supported the in vitro enzymatic inhibition assays results. Thus, 9b and 13d are potent anti-breast cancer benzoxazoles with selective ARO and PI3kα inhibition activity, respectively, while 6, 9a, and 13b are multi-target inhibitors exhibiting other anticancer synergistic mechanisms.

The signature integrates non-invasively detected sEV RNAs to complement LDCT, addressing its high false-positive rate, and offers prognostic insights for personalized treatment strategies. These findings highlight the clinical potential of sEV-derived long RNAs in early LUAD detection and precision oncology.

This study elucidates the molecular mechanisms by which ginseng exerts its therapeutic effects on IS. The identification of key active ingredients and their targets offers new insights into the development of effective treatments for IS.

Dasatinib, an FDA-approved SRC/EPHA2 inhibitor, effectively reduced p-PI3KβY962 and inhibited tumor progression in PTEN-null but not PTEN-WT tumors. These findings establish p-PI3KβY962 as a druggable target and biomarker for developing targeted therapy in PTEN-deficient cancers beyond conventional PI3K kinase inhibition.

Additionally, PDGFRA, a downregulated hub gene, demonstrated strong interactions and may serve as a tumor suppressive target modulated by these glycosides. The online version contains supplementary material available at 10.1007/s40203-025-00461-y.

The PI3K inhibitors GDC-0032 and INK1117 for PI3K-α and AZD8186 for PI3K-β are now being studied in clinical trials. Research on the clinical development, therapeutic utility, and structural insights of new PI3K inhibitors is the main emphasis of this review. The inhibitors have been shown promising anticancer activity relationships.

P1, N=23, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Oct 2025 --> Oct 2026

This finding suggests that PhenDC3 may induce DNA replication stress in this cell line. Collectively, these results support the feasibility of employing canine cancer cells as a model system to investigate the role of G-quadruplex structures in cancer.