ASF1B overexpression

Treatment with thiostrepton, a FOXM1 inhibitor, not only suppressed ASF1B expression, but also inhibited GC progression...The crucial role of ASF1B-regulated PRDX3 in GC cell proliferation and oxidative stress balance was also elucidated. In summary, our study suggests that the FOXM1-ASF1B-PRDX3 axis is a potential therapeutic target for treating GC.

Collectively, our findings identify the TLK1-ASF1 pathway as a novel mediator of inflammatory signaling and a promising therapeutic target for AML treatment across diverse genetic subtypes. Selective inhibition of this pathway offers potential opportunities to intervene effectively, address intratumoral heterogeneity, and ultimately improve clinical outcomes in AML.

ASF1B was associated with tumor immunity. In summary, ASF1B may promote malignant behavior of LUAD cells, and its overexpression correlates with worse prognosis and better immunotherapy effect.

Moreover, STAD patients with high ASF1B expression had a higher tumor mutation burden score, microsatellite instability score, PD-1 immunophenoscore, and immune checkpoint expression. Our results suggest that ASF1B was an independent prognostic factor for STAD as well as a potential target for immunotherapy.

The AUCs of the 1-year, 3-year, and 5-year survival-related ROC curves were 0.672, 0.590, and 0.591, respectively. Our study shows that ASF1B may provide new ideas for the diagnosis and prognosis of liver cancer patients, as well as providing a new direction for the application of ASF1B in tumour immunotherapy.

Overexpression of Myc reversed the inhibitory effect of ASF1B silencing on AGS cell proliferation, invasion and cisplatin resistance. In conclusion, the results indicate that knockdown of ASF1B may suppress GC cell proliferation, migration and invasion, and promote cell apoptosis and cisplatin sensitivity by modulating the Myc pathway, thereby offering novel possibilities for reversing cisplatin resistance in GC.

ASF1B deficiency obstructed the proliferation, cell cycle as well as metastasis of LGG cells, and induced cell death, which might be realized through the interaction with TLK1. The interaction between ASF1B and TLK1 promoted the malignant progression of LGG.Key messagesTLK1 interacts with ASF1B.Interference with ASF1B inhibits the proliferative, invasive and migratory capabilities and induces the cycle arrest, along with the apoptosis of LGG cells.The interaction between ASF1B and TLK1 promotes the malignant progression of LGG.

Our study demonstrates that circCDK17 regulates the expression of ASF1B by miR-122-5p competition and thus promotes the development of CC, providing a novel targeted therapy for CC.

Additionally, increased caspase (caspases-3 and -9) activation and PARP cleavage led to enhanced caspase-dependent apoptosis and improved cisplatin sensitivity. Collectively, our results indicate that ASF1B may serve as a potential biomarker of pancreatic cancer and a novel therapeutic target.

Additionally, ASF1B silencing suppressed the PI3K/Akt pathway and 740Y-P treatment partially abolished the effects of ASF1B knockdown on PC cells. In conclusion, ASF1B silencing retarded proliferation and promoted apoptosis in PC cells by inactivation of the PI3K/Akt pathway.

Patients who received anti-PD-L1 immunotherapy with high ASF1B expression had a higher objective response. The ASF1B level is an independent prognostic factor and may serve as a potential immunotherapeutic target.