PKD2 (Polycystin 2)

PKD2 plays a crucial role in human neutrophil survival. Minimizing PKD2 inhibition during small-molecule drug design could be essential to reduce the risk of neutropenia in patients under anti-cancer treatment.

P4, N=80, Completed, China-Japan Friendship Hospital; China-Japan Friendship Hospital

The results of this study indicate the potential involvement of polycystins in the pathogenesis of astrocytomas. However, further research is required to fully understand the mechanisms that these molecules are implicated.

Tolvaptan was initiated, and he remains under follow-up. Mutations in the PKD1/PKD2, which are responsible for ADPKD, affect intracellular signaling, including the mammalian target of the rapamycin (mTOR) pathway, leading to cyst formation and progression, while NF1 mutations overactivate the Ras proteins. His disease progression was more severe than that of his father with ADPKD alone, suggesting NF1 may have accelerated cyst enlargement. The co-occurrence of ADPKD and NF1 is extremely rare, with only a few cases reported in the past.

P1/2, N=116, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology; Tongji Hospital, Tongji Medical College, Huazhong University o

However, the role of PKD3 was elusive in some cancers. Our findings suggest that testing for PKD isotypes with immunohistochemistry may support the diagnostic estimation of tumor progression and prognosis in HNSCC with a potential therapeutic relevance.

Lastly, the observed alterations in the CD8+ T cell compartment did not impact proper immune response upon immunization with ovalbumin or in a subcutaneous tumour model suggesting only a small to absent biological relevance. Taking together the knowledge of all our published studies on PKD3 in the T cell compartment, we now conclude that T cell-intrinsic PKD3 is a fine-tuner of central memory T cell as well as CD8 single positive thymocyte development.

Efforts to improve CRISPR-Cas technologies involve optimizing delivery vectors, employing viral and non-viral approaches and minimizing immunogenicity. With research in animal models providing promising results in rescuing the expression of wild-type podocin in mouse models of nephrotic syndrome and successful clinical trials in the early stages of various disorders, including cancer immunotherapy, there is hope for successful translation of genome editing to kidney diseases.

We found PKD2 was highly expressed in LUAD and silencing PKD2 could promote erastin-induced reactive oxygen species (ROS), malondialdehyde (MDA) accumulation, intracellular iron content and LUAD cells death...PKD2 knockdown or pharmacological inhibition by CRT0066101 could enhance efficacy of carboplatin in LUAD via ferroptosis and apoptosis. Collectively, our study revealed that abrogation of PKD2 could aggravate ferritinophagy-mediated ferroptosis by promoting autophagosome-lysosome fusion and enhance efficacy of carboplatin in LUAD. Targeting PKD2 to induce ferroptosis may be a promising strategy for LUAD therapy.

Mechanistically, PKD2 and PKD3 positively regulated Runx2 via MAPK/ERK1/2 pathway and promoted EOC. Taken together, our results indicated that PKD2/3/ERK1/2/Runx2 signalling axis might be a novel drug target against EOC and CRT0066101 could be developed as a promising therapeutic choice against this lethal pathology.

Moreover, circPKD2 could target miR-1278 to up-regulate LATS2 expression to suppress the cell proliferation, invasion, and glycolytic metabolism. These findings display that circPKD2 can function as a tumor suppressor in glioma by controlling the miR-1278/LATS2 axis and provide the potential biomarkers for glioma treatment.