PIP5K1C (Phosphatidylinositol-4-Phosphate 5-Kinase Type 1 Gamma)

We also observed the upregulation of matrix metalloproteinase (MMP) genes and components of the glycosaminoglycan degradation pathway in glioma cells on the collagen matrix compared with those on HA matrix. This study reveals the effect of collagen and HA on glioma cells at the transcriptional level and contributes to the understanding of potential targets for therapy.

Furthermore, six potential therapeutic agents for EC were identified: BIRB.0796, Camptothecin, CHIR.99021, Methotrexate, PF.4708671, and Vorinostat. Furthermore, several potential therapeutic agents for EC were identified, offering promising avenues for treatment. These findings hold significant potential for enhancing the survival outcomes of EC patients and provide meaningful guidance for clinical decision-making in managing this malignancy.

We then applied the model to simulate signaling perturbations linked to PI4KA and PIP5K1C loss-of-function, two lipid kinases associated with neurodevelopmental and neuromuscular disorders. This modeling framework provides a scalable foundation for predictive biochemical modeling and offers a path toward individualized applications in precision medicine.

Notably, our study identified eight drugs-Bortezomib, Midostaurin, CHIR.99021, JNK.Inhibitor.VIII, Lenalidomide, Sunitinib, GDC0941, and GW.441756-as exhibiting sensitivity toward OS. The outcomes of this investigation present an opportunity to predict the survival outcomes among individuals diagnosed with OS. Furthermore, these findings hold promise for progressing research endeavors focused on prognostic evaluation and therapeutic interventions pertaining to this particular ailment.

Compounds 30 and 33 not only showed potent activity but also demonstrated low total clearance in mice and high levels of kinase selectivity. These compounds might serve as tools to further elucidate the complex biology and therapeutic potential of PIP5K inhibition.

Functional analysis revealed their involvement in cancer cell migration and invasion mechanisms, providing valuable insights for the development of future anti-CRC drugs. We successfully identified five CRC risk genes, providing new insights and research directions for the effective mechanisms of CRC.

In summary, miR-4649-5p exerts broad tumor-suppressive effects in TNBC and shows potential for combined therapeutic approaches targeting the PIP5K1C/PI3K/AKT signaling axis.

We also identified the significant impact of KRAS, P53, and CDKN2A mutations on the prognosis of this fatal disease. Therefore, our study highlights the crucial role of anoikis in the development of the pancreatic adenocarcinoma tumor microenvironment.

It gave a precision of 91.3% and 91% recall after fine tuning. Some of the common biomarkers predicted for NSCLC and SCLC were CDK4, CDK6, BAK1, CDKN1A, DDB2.

Additionally, results in both univariate and multivariate Cox regression analysis confirmed the well prognosis efficacy of the prediction model (both P < 0.001). Moreover, a potential splicing regulatory network was established and after multiple-database validation, we supposed that the signaling axis of HSPB1 up-regulating the PIP5K1C - 46,721 - AT (P < 0.001) might mediate the tumorigenesis, progression and metastasis of PRAD via the key members of Alzheimer's disease pathway (SRC, EGFR, MAPT, APP and PRKCA) (P < 0.001).

We constructed a prognostic model containing eight cuproptosis-related genes (AKR1B10, KLHL29, PROM2, PIP5K1C, KIF18B, AMIGO2, MRPL3, and PI4KB) that can accurately predict the prognosis of PAAD patients. The results will provide new perspectives for individualized outcome prediction and new therapy development for PAAD patients.