CHKA (Choline Kinase Alpha)

CHKA drives glioma malignancy by regulating EGFR and activating the MAPK pathway. The CHKA/EGFR/MAPK axis represents a potential therapeutic target for glioma treatment.

In addition, the downregulation of CHKA can decrease the expression of PFKM and inhibit its activity, thereby blocking the Warburg effect. These observations shed new light on the antitumor mechanisms of CQ and provide new evidence for the close relationship between the PI3K/AKT signaling pathway and the Warburg effect, providing new therapeutic targets for treating CRC.

Notably, exosomes derived from glioma cells with normal CHKA expression exhibit a greater capacity to promote glioma progression compared to those derived from cells with low CHKA expression. Overall, our findings suggest that CHKA modulates exosome secretion via an autophagy-dependent pathway, thereby facilitating the proliferation, migration, and invasion of glioma cells.

PC accumulation impairs the proliferation ability and stem cell characteristics of EC cells by inhibiting the activated mTOR-c-Myc axis, potentially offering a promising strategy to enhance the efficacy of EC clinical therapy through the promotion of PC accumulation in tumor cells.

Treatment with abiraterone or enzalutamide in metastatic castrate-resistant prostate cancer patients elicited mixed responses on PET at 12-16 weeks despite predominantly stable radiological appearances. The sum of the weighted tumour-to-background ratios (TBRs-wsum) was associated with the duration of survival.

Tumours with strong CKα expression are reportedly highly active in breast cancer. A correlation was observed between CKα expression and C-choline accumulation, suggesting their role as prognostic indicators of breast cancer.

Metabolomics and transcriptomic analysis allow us to discriminate MAFLD-HCC according to fibrosis severity. Our findings identified that CHKA and MBOAT7 could be proposed as biomarkers to MAFLD-HCC patients without or with low level of fibrosis. In addition, the different expression of CHKA support the idea that choline could be used as a more efficient tracer of PET-scan in MAFLD-HCC patients.

Finally, the molecular docking simulation suggested that picrasinoside F and luteolin in dandelion extract had the most highly binding scores with CHKA, indicating they may be the potential CHKA inhibitors to regulate glycerophospholipids metabolisms of TNBC. In conclusion, we confirmed the antitumor effects of dandelion extract against TNBC cells in vitro and demonstrated that dandelion extract could interfere with glycerophospholipids and unsaturated fatty acids metabolism via downregulating the CHKA expression and inhibiting PI3K/AKT/SREBP/FADS2 axis.

These findings support the role of MALAT1 as a CHKA activator through putative association with the liganded or unliganded AR, unveiling its targeting as a therapeutic option from a metabolic rewiring perspective.

We observed a significant increase in NP delivery and a significant decrease in Chkα and phosphocholine in VEGF overexpressing xenografts. Our results demonstrated the importance of tumor vascularization in achieving effective siRNA delivery and downregulation of the target gene Chkα and its function.