HPGD (Hydroxyprostaglandin dehydrogenase 15-(NAD))

Overall, this study elucidates the intricate interplay between these cfRNAs in the CRC prognosis. The results advocate for further exploratory studies to validate PACS1's potential as a prognostic marker and reinforce the clinical significance of HPGD and TDP2 in the context of CRC management, positioning them as vital elements in the landscape of molecular oncology.

The results demonstrate that 15-PGDH suppresses CC cell proliferation and migration by downregulating the Notch1 signaling pathway. These findings provide new insights into the molecular mechanisms underlying CC and suggest 15-PGDH as a promising therapeutic target.

Furthermore, the qPCR results from LUAD cells treated with DNA methylation and histone deacetylase inhibitors indicated that low expression of GPM6B was associated with DNA methylation and histone deacetylation. Overall, the present study demonstrated that GPM6B may serve as a novel tumor suppressor and elucidated its potential mechanism in regulating the progression of LUAD.

With specific PGE2 receptor inhibitors, AH6809 significantly affects the proliferation and migration of LNCaP cells with high ACSM1 expression. Based on our results, it appears that ACSM1 regulates prostate cancer cell behavior via the 15-PGDH-mediated PGE2 signaling pathway and Extracellular Matrix (ECM) remodeling.

The USP20 expression is significantly upregulated in CRC, and can promote tumor metastasis by affecting immune cell infiltration. As an important tumor metabolite which can influence immune cell infiltration, PGE2 is regulated by USP20 through the protein degradation of mPGES-1 and 15-PGDH mediated by proteasome.

Low HPGD expression was linked to resistance to certain chemotherapies, potentially due to immunosuppression triggered by low HPGD levels. Validation in clinical samples from the local hospital confirmed the decreased 15-PGDH expression and increased COX-2 expression in HPV16-positive cervical cancer patients and increased immune suppression during cancer progression.ConclusionsHPGD/15-PGDH is a potential biomarker for predicting the progression, immune response, and chemotherapy sensitivity of cervical cancer, with implications that it is of great value for the diagnosis and individual-based treatment of cervical cancer.

Congruently, patients and mice resistant to αPD1 fail to suppress HPGDS in TAMs, reinforcing the evidence that circumventing HPGDS is necessary for efficient αPD1 treatment. Overall, we disclose a mechanism whereby T-cell activation controls the innate immune system, and we suggest HPGDS/PGD2 targeting to overcome immunotherapy resistance.

These findings suggest that HPGD may exert its tumorigenic effects through non-enzymatic mechanisms, potentially by involving modulation of KRAS signaling in human TNBC cells. Our results highlight the diverse roles of HPGD in cancer biology, particularly in the context of TNBC, and point to non-enzymatic pathways as a significant aspect of its tumorigenic activity.

This article provides insights and comprehensive overview of the tumor suppressor role of 15-PGDH in various cancers. Epigenetic and post-translational mechanisms regulating 15-PGDH expression and the role of novel ROS-Nrf2-15-PGDH axis upstream of 15-PGDH expression were discussed and accented as potential drug targets.

P=N/A, N=40, Completed, Shang Panfeng

VDR expression correlated positively with PGE2 and COX-2 but negatively with 15-PGDH. No associations were found between these factors and therapy outcomes.