PTPRG (Protein Tyrosine Phosphatase Receptor Type G)

Sequencing data show that PTPRG knockdown is associated with the activation of metabolism-related pathways and altered expression of the transcription factor-coding gene prospero-related homeobox 1 (PROX1). These findings identify PTPRG as a novel negative regulator of axonal regeneration, expanding the repertoire of molecules that can be manipulated to improve functional recovery after nerve injuries.

We analyzed 103,171 single-cell transcriptomes from 18 MM samples (10 optimal responders [OR] and 8 suboptimal responders [SOR] to bortezomib-melphalan-prednisone) to investigate cell-type composition, malignant plasma cell subclusters, and tumor-microenvironment crosstalk. In contrast to the known role as a tumor suppressor in solid and hematologic cancers, our integrative analyses identified PTPRG among seven stemness-related genes upregulated in MalPlasma3 and poor-survival cells, which was echoed in the observed reduced cell viability and increased apoptosis in MM cell lines following siRNA-mediated PTPRG knockdown. This single-cell multi-omic dissection implicates a proliferative, stem-like MalPlasma3 subcluster and identified PTPRG as a key mediator of drug resistance and poor outcome in MM, offering novel prognostic biomarkers and therapeutic targets.

This review also includes gene editing to target oncogenic drivers or correcting mutations and USP inhibition to overcome resistance. Finally, it concludes by emphasizing the importance of combining these diverse therapeutic approaches with ongoing next-generation TKIs and comprehensive and personalized approaches for CML treatment, offering a path toward deeper remissions and ultimately achieving curative outcomes for CML patients.

PTPRG may restrict the cell proliferation and migration and can restore the miR-23b mediated CRC growth. MiR-23b is directly linked with the CRC development via PTPRG restriction suggesting miR-23b as novel therapeutic target against CRC.

This research has improved our understanding of lymphoma, especially those occurring in atypical sites, and reshaped our concept of lymphoma classification and management. We suggest considering incorporating PA-LBCL into IP-LBCL in the future classification of lymphoma.

These findings are consistent with existing literature, suggesting that identified methylation features likely contribute to AML progression through alterations in gene expression levels. Therefore, this study provides a valuable reference for enhancing recurrence risk prediction models in AML and clarifying disease pathogenesis, as well as offering broader insights into mechanisms underlying other major diseases.

Finally, we constructed GC cell models with PTPRG-AS1 overexpression or knockdown and GC liver metastasis models and found that PTPRG-AS1 can sponge hsa-miR-421, releasing KITLG and promoting GC proliferation and metastasis through the KITLG/KIT pathway. Taken together, CKI can suppress these malignant phenotypes by regulating the PTPRG-AS1/hsa-miR-421/KITLG axis.

RAF1-rearranged spindle cell neoplasm encompasses a morphologically and molecularly diverse spectrum of mesenchymal tumours occurring in both children and adults. We describe an ileal lesion and two novel SPPL2A::RAF1 and ERC1::RAF1 fusions to further expand its clinicopathological and genetic spectrum.

USP1 mRNA stability was determined after actinomycin D treatment...HOXA10 downregulation inhibited in vivo NPC proliferation through the PTPRG-AS1/USP1 axis. In conclusion, HOXA10 facilitates NPC cell proliferation in vitro and in vivo through the PTPRG-AS1/USP1 axis.

Collectively, the study demonstrates that lncRNA PTPRG-AS1 may act as a competing endogenous RNA by regulating the miR-4659a-3p/QPCT axis in BRCA progression. This lncRNA could potentially be a biomarker and therapeutic target for BRCA.

The diversity of RPTPγ and RPTPζ splice variants likely corresponds to distinct signaling functions, in different cellular compartments, during development vs later life. In contrast to previous studies that report divergent RPTPγ and RPTPζ protein expressions in neurons and sometimes in the glia, we observe that RPTPγ and RPTPζ co-express in the somata and processes of almost all HC neurons but not in astrocytes, in all three HC preparations.

Moreover, decreases in copy numbers of GBP-1, MIR3141, OR5P1E, and PTPRG relative to those in healthy cattle were also observed. Because DNA copy number variation represent a major contribution to the somatic mutation landscapes in human tumors, these findings suggest that DNA copy number changes might have contributed to the onset of DLBCL in the present case.