PLK2 (Polo Like Kinase 2)

Bioinformatics analysis demonstrated high PLK2 expression was positively associated with oncogenes such as FAM163A, CTNND2, DAAM2, PITX1, POU1F1, mir-196a and negatively associated with tumor suppressors such as EMX2, PADI3, CDO1, SHOX2 and mir-508. In conclusion, the research elaborates on the expression profile and the clinical significance of PLK2 gene in AML, suggesting PLK2 expression may help risk stratification and hypothesis-generating for HSCT decision support.

In conclusion, FAM117B promoted the pathological progression of CRC through enhancing the DYRK1A/PLK2 signaling pathway. Our study provided insights for potential therapeutic strategies against CRC.

Low PLK2 expression is strongly associated with postoperative seizure recurrence, synaptic dysfunction, and neuroinflammation, suggesting its use as a predictive biomarker and therapeutic target in GRE.

This study established a robust six-gene prognostic model related to SUN modifications and anti-PD-1 therapy in GBM. The model demonstrates strong predictive ability and correlates with clinically relevant parameters, highlighting its potential utility for survival prediction and guiding therapeutic management decisions in GBM patients.

Our study highlights the prognostic value of the PLK gene family in glioma and identifies PLK2 as a promising therapeutic target. The PLK2 inhibitor ON1231320 shows potential as an anti-GBM agent and warrants further investigation in preclinical and clinical studies.

This study establishes PLK2 as a key regulator of glycolysis and immune imbalance in PCOS, highlighting its pivotal role in the metabolic-immune crosstalk within the ovarian microenvironment. These findings suggest that targeting PLK2 may be a potential therapeutic strategy for alleviating glycolytic dysregulation and chronic inflammation in PCOS.

It also covers recent insights into the conformational regulation of other members of the Polo-Like kinase family. The implications of the conformational regulation of PLK1 with respect to cell cycle function and drug discovery are significant and are therefore discussed in detail.

Oral administration of blood-brain barrier-penetrable MEK1/2 inhibitors lowered pathological αsyn and rescued PD-relevant phenotypes with an acceptable safety profile in these mice. Collectively, these data highlight MEK1/2 inhibitors as a potential therapeutic strategy for PD.

Additionally, we speculated that As-induced the elevation of USP7 expression due to the excessive inflammatory cytokines secretion and the activation of mTORC1/WTAP pathway. These findings offer novel insights into the molecular mechanisms underlying As-mediated lung cancer.

Hence, the anti-proliferative effects of leflunomide on prolactinoma cell lines may be mediated through programmed cell death pathways. Importantly, combining cabergoline with leflunomide effectively enhances the toxic effect of cabergoline, suggesting a potential therapeutic role for leflunomide in drug-resistant prolactinoma.

Doxorubicin (DOX), a chemotherapeutic drug used for cancer treatment, faces limitations in clinical use due to its cardiotoxicity...MiR-27b-3p negatively regulated the expression of four target genes (Plk2, Adora2b, Apaf1 and Nrk) in DOX-stimulated cardiomyocytes. In conclusion, miR-27b-3p ameliorates DOX-induced cardiac dysfunction and myocardial injury by inhibiting inflammation and oxidative stress.

However, further efforts are necessary to validate their clinical value for diagnosis and prognosis and to develop practical applications in clinical settings. Nevertheless, these pan-cancer profiles offer a better overall understanding as well as useful information for future reference regarding mitotic DNA integrity checkpoint signaling in cancer.