CNPY2 (Canopy FGF Signaling Regulator 2)

This study uncovers key genes and signaling pathways in the prostate cancer tumor microenvironment, particularly genes such as CNPY2, CPE, DPP4, IDH1, NIPSNAP3A and WNK4, which have potential as therapeutic targets. Our findings provide new insights into personalized treatment strategies for PCa and warrant further clinical validation in the future.

After PRRT4 knockdown, the proliferation ability of THP1 cells was significantly enhanced, and the apoptosis ratio was significantly decreased. PRRT4 may serve as a potential therapeutic target and prognostic marker for various malignancies.

These findings suggest that LRRTMs may have functions beyond their established role in excitatory synapse development, such as the regulation of neurotransmission and behavior. Targeting LRRTM4 therapeutically may thus be an interesting novel approach to alleviate excessive aggression or anxiety associated with a number of neuropsychiatric conditions.

This review underscores the need for further research to fully elucidate CNPY2's oncogenic mechanisms and develop targeted therapies. Improved understanding of CNPY2's diverse roles may lead to novel diagnostic and therapeutic approaches in solid tumors.

CNPY2 is markedly overexpressed in NSCLC and is associated with increased tumor aggressiveness and EMT. Serum CNPY2 shows promise as a non-invasive biomarker for NSCLC diagnosis, and elevated expression is correlated with a poorer prognosis. Thus, CNPY2 may serve as both a valuable biomarker and a potential therapeutic target in NSCLC.

Cnpy2 knockout inhibits NFκB2/p52-mediated transcription of Flt1 and Kdr in macrophages. These findings demonstrate that CNPY2 regulates macrophages in both inflammation and hepatocarcinogenesis and may serve as a therapeutic target for cancer.

They are involved in a wide range of diseases, including angiogenesis, abnormal immune responses, neurodevelopmental disorders, and the development of tumors. Here, we summarized the biological processes and influence on the disease of every CNPY family protein to elucidate potential biomarkers and point out the direction for future in-depth research.

These results demonstrate that CNPY2 is expressed by corticostriatal neurons involved in the regulation of movement. CNPY2 enhances neuronal survival by reducing ER stress and is a promising factor to consider in HD and possibly in other brain diseases.

In addition, the paper also details the biological functions and roles of canopy FGF signaling regulator 1 (CNPY1), canopy FGF signaling regulator 3 (CNPY3), canopy FGF signaling regulator 4 (CNPY4), and canopy FGF signaling regulator 5 (CNPY5). The mechanism and function of CNPY2 should be continued to study in order to accelerate disease prevention in the future.

In summary, we concluded that persistent TCR stimulation and the tumor microenvironment induce CNPY2 expression and UPR in CD8+ T cells. However, ablating CNPY2 alone failed to overcome UPR-mediated T cell dysfunction, suggesting that targeting multiple initiators of UPRs in CD8+ T cells need to be considered  to improve cancer immunotherapy.

This study revealed that the TENM4 (p.P421L) pathogenic missense variation was responsible for ET in the proband.

In conclusion, PRC2 and its epigenetic effects are major oncogenic mechanisms underlying both bladder cancer and UTUC. The epigenetically regulated genes of PRC2 in urothelial carcinoma were also elucidated using correlation statistics.