QPCT (Glutaminyl-Peptide Cyclotransferase)

In conclusion, QPCT promotes tumorigenesis in LUAD by increasing macrophage recruitment and M2 macrophage proportion. This may be due to FTO-mediated demethylation increasing the QPCT mRNA stability.

We also discuss the possible therapeutic implications of targeting QPCTL in cancer therapy. QPCTL is a prospective target for the development of innovative anticancer treatments due to its participation in several cancer-associated pathways.

Bioinformatics and machine learning techniques identified the common genes "RXRG, CDH2, ETV5, QPCT, LRP4, FN1, and LPAR5" as PTC biomarkers, providing novel reference markers for the diagnosis and treatment of PTC patients. The model is anticipated to possess significant predictive value and assist in the early diagnosis and screening of clinical PTC. These insights enhance the field of PTC management and offer guidance for future research.

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.

Therefore, MTDH/NF-κB (p65)/QPCT signal axis was proposed. Collectively, our findings delineate the mechanism by which the MTDH/NF-κB (p65) axis regulate QPCT signaling and suggest that this complex may play an essential role in breast cancer progression and affect DOX sensitivity.

SC-2882 is a first-in-class specific QPCTL inhibitor that induces secondary proteolytic degradation of the monocyte chemoattractants CCL2 and CCL7 (da Silva, Nature Immunology 2022) and inactivation of the "do-not-eat-me" signal CD47 (Logtenberg, Nature Medicine 2019)...Additional analysis of LME cell subpopulations by SC-RNA-seq is ongoing. Overall, these data indicate that QPCTL is a potential target in DLBCL, and that QPCTL inhibition exhibits potent anti-lymphoma effects primarily by targeting the IN-LME.

Our data represent an additional step for refining the molecular taxonomy of I-NET, identifying novel transcriptome subgroups with different biology and therapeutic opportunities.

ISM8207 (10 mg/kg BID) combined with rituximab resulted in synergistic effects in the B-NHL xenografts. ISM8207 was well-tolerated with favorable ADME and PK properties. Conclusions These data strongly support the clinical evaluation of ISM8207 as a novel cancer immunotherapy in TNBC and B-NHL.

Functional study and rescue assay demonstrated that QPCT depletion further promotes cell proliferation, inhibits apoptosis and impairs myeloid differentiation of AML cells, alleviating the anti-leukemic effect of Apicidin on AML. Our findings not only provide novel therapeutic target for AML, but also lay theoretical and experimental foundation for the clinical application of Apicidin in AML patients.

We found an eight-gene signature associated with a higher risk of rapid relapse after treatment in patients with oligodendrogliomas. This finding could help clinicians identify patients who need more intensive treatment.

QPCT, SCEL and TNFRSF12A are expected to be diagnostic markers for PTC.