PTPRN (Protein Tyrosine Phosphatase Receptor Type N)

The TMEM59L/PTPRN axis is a key regulator of DDR and 5-FU resistance in CRC. TMEM59L promotes chemoresistance via PTPRN by enhancing DNA repair and reducing ROS-mediated apoptosis. Targeting this pathway may offer a novel strategy to overcome 5-FU resistance.

This study found 8 genes that have been implicated in primary tumors or metastasis of other cancers which require further investigation into their involvement of metastasis in melanoma.

Additionally, 5Z-7-Oxozeaenol upregulated the pro-apoptotic proteins p53 and cleaved caspase-3. In conclusion, 5Z-7-Oxozeaenol exerts potent antitumor effects on MDA-MB-231 cells through multi-pathway inhibition and induction of apoptosis, highlighting its potential as a marine-derived therapeutic candidate for breast cancer treatment.

Among these genes, MMP9 and SNAI1 are core genes that link PTPRN and the epithelial-mesenchymal transition (EMT) pathway. PTPRN, a key molecule associated with the EMT pathway, can be used as a molecular marker for tumor risk assessment, detection, and diagnosis in the early stages of glioma.

Finally, we found that FB slowed down the growth of tumor in a GBM orthotopic mice model through upregulating PTPRN expression in vivo, with no significant toxicity to other organs. Taken together, these results suggest that FB exerts its anticancer effects on GBM via increasing the expression of PTPRN, which may provide a potential new therapeutic strategy for the treatment of GBM.

The DMC biomarker found for the HER2+ subtype, hypermethylation in the PTPRN2 gene (cg25910261), has the potential to be used by healthcare providers to identify HER2+ patients and provide the HER2-targeted therapy to improve the patient's survival. In addition, our developed MSP method could produce an effective diagnostic tool for classifying the Luminal A and Luminal B subtypes, with accuracies of 75% and 76%, respectively.

The combination of ALX3, NPTX2, and TRIM58 was selected from distinct functional groups. An accuracy prediction of 93.3% could be achieved by validating the ten most common cancers, including the initial five low-survival-rate cancer types.

These findings hold significant potential to refine treatment strategies, and enhance survival outcomes for NSCLC patients. By enabling a personalized therapeutic approach tailored to individual risk scores, this model may facilitate more precise decisions concerning immunotherapy and chemotherapy, thereby optimizing patient management and treatment efficacy.

OPISV is feasible for predicting patient survival, as it may serve as a potential mechanism underlying the involvement of GABAergic synapses in the progression of GBM.

The nomogram showed that the prognostic risk model was reliable and that the accuracy of predicting survival in each patient was high. The prognostic risk model can effectively classify patients with glioblastoma into high-risk and low-risk groups in terms of overall survival rate, which may help select high-risk patients with glioblastoma for more intensive treatment.

We describe the immunologic microenvironment on PRAD tumors with a high expression of KLK2, including a gene signature linked with an inert immune microenvironment, that predicts the response to ICIs in other tumor types. Strategies targeting KLK2 with T cell engagers or antibody-drug conjugates will define whether T cell mobilization or antigen release and stimulation of immune cell death are sufficient effects to induce clinical activity.

Elevated pERK staining in tumor cells provided evidence of activated mitogen-activated protein kinase (MAPK) signaling. This report raises the possibility that gene fusion events may be involved in meningioma pathogenesis and warrant further investigation.