PTPRF (Receptor-type tyrosine-protein phosphatase F)

Our analysis delineates a plausible link between DIGs and DLBCL outcome, nominating CCT5 as environmentally relevant biomarkers with prognostic and potential therapeutic implications.

qRT-PCR and Western blot confirmed PTPRF, ULK1, TGM3, and CRABP2 were upregulated at both the mRNA and protein levels. These findings indicate that the Treg-related signature serves as robust prognostic biomarkers and may guide personalized immunotherapy in SCKM.

Because PTPRD functions are pathway-specific and shaped by mini-exon usage or redundancy with other family members (PTPRS/PTPRF), domain- or ligand-selective interventions represent plausible therapeutic strategies. Elucidating its full ligand repertoire, substrate landscape, and structural basis for allosteric regulation will be critical for converting this versatile receptor from a mechanistic curiosity into a tractable target for neurodevelopmental, neuropsychiatric, and metabolic disorders.

Methyl-angolensate, byssochlamic-acid, homoharringtonine, piperacillin and cephaeline were potentially targeted therapeutic compounds for hub genes based on molecular docking. Our study firstly provides new insight into the genetic crosstalk between metastatic melanoma and vitiligo that may facilitate the development of personalized treatments.

Our integrative single-cell and bulk-RNA workflow identifies ANLN, NT5E, and CTSV as novel prognostic biomarkers in pancreatic cancer and highlights a pro-tumorigenic interaction between malignant ductal cells and macrophages. Targeting CTSV or disrupting CXCL14-CXCR4 and IL1RAP-PTPRF signaling may offer new therapeutic avenues for PAC.

We identify galectin family proteins as uniquely enriched in trastuzumab-resistant models, and show that genetic and pharmacological inhibition of galectins restores trastuzumab sensitivity...We also identified protein tyrosine phosphatase F (PTPRF) as a pan-cancer HER2 interactor, which is broadly upregulated and whose knockdown suppresses proliferation in HER2-low cancers. This work provides an extensive new interactomic resource and underscores the utility of proximity labeling for mapping complex cancer networks and identifying new therapeutic targets.

Models for predicting the OS and PFS were successfully established and validated. The models may help to establish the personalized therapeutic strategies before treatment.

Furthermore, based on angstrom accuracy of the DNA duplex, the maximum catalytic radius of PTPRF was determined as ∼25.84 nm, providing a basis for the development of phosphatase-recruiting strategies. Taken together, our study provides a generic methodology not only for selectively mediating RTK phosphorylation and cellular biological processes but also for developing novel therapeutic drugs.

Analysis of cytokine released from Jurkat E6.1 T cells co-cultured with GluIIß knockout A549 cells showed significant increased level of angiogenin and significant decreased level of ENA-78. In conclusion, knockout of GluIIß from cancer cells induced altered gene expression profile that improved anti-tumor activities of co-cultured T lymphocytes and PBMCs thus suppression of GluIIß may represent a novel approach of boosting anti-tumor immunity.

KRAS proto-oncogene, GTPase (KRAS)-mutated MDA-MB-231 cells were more resistant to trametinib upon PPFIA1 knockdown compared with control cells...Furthermore, liprin-α1 depletion led to more pronounced redistribution of RAS proteins to the cell membrane. Our data suggest that liprin-α1 is an important contributor to oncogenic RAS/MAPK signaling, and the status of liprin-α1 may assist in predicting drug responses in cancer cells in a context-dependent manner.

Sarcopenia may be related to immunosuppressive microenvironment and affect the prognosis of AML patients.

The signaling landscape that accompanies Ephexin3 in various cancer types included the tyrosine kinase receptor MET and the tyrosine phosphatase receptor PTPRF, the serine/threonine kinases MARK2 and PAK6, the Rho GTPases RHOD, RHOF and RAC1, and the cytoskeletal regulator DIAHP1. Our findings set the basis to further explore the role of Ephexin3/ARHGEF5 as an essential effector and signaling hub in cancer cell migration.