KLF10 (Kruppel Like Factor 10)

FBXO22 promotes pancreatic cancer progression by mediating KLF10 ubiquitination and degradation, thereby impairing its tumor-suppressive functions. FBXO22 may serve as a potential oncogenic and therapeutic target associated with pancreatic cancer progression.

Core circadian genes represent promising candidate biomarkers for both cancer survival risk stratification and immunotherapy response prediction. They further enable the development of high-accuracy machine learning models to predict immunotherapy responses.

This study developed a model for predicting OS in NBL by integrating Schwann cell-specific genes, clinical factors, and the TME. The model highlights the importance of specific cellular contributions to prognosis and provides a more personalized approach to NBL treatment, particularly for high-risk patients.

In aged individuals, elevated levels of MMA in the blood induce the activation of the KLF10/SP1‒LOXL2 axis in PSCs to increase linear ECM alignment. Following the initiation of pancreatic cancer, this increased linear ECM alignment leads to increased tumor invasion into surrounding tissues, resulting in a greater proportion of stage T3/T4 tumors and a greater incidence of LVI and PNI in aged patients, ultimately leading to poorer outcomes (This schematic was created with www.figdraw.com ,export id: PRPRS4e268).

The role of autophagy in ESM1 regulation on lipid metabolism was explored using autophagy inhibitor chloroquine (CQ). Co-IP, dual-luciferase reporter assay, actinomycin D treatment assay, and others were used to analyze the mechanism of ESM1 regulation on lipid metabolism...High expression of ESM1 predicted poor prognosis in OC patients. ESM1 regulated lipid metabolism through IGF2BP3/ESM1/KLF10/BECN1 positive feedback, which was a promising target for OC treatment.

This multi-omics study provides insights into the asthma-lung cancer link and presents a promising prognostic model for lung cancer based on asthma-related genes. The model's association with immune features suggests its potential utility in immunotherapy patient selection.

Thus, we postulate that KLF10 is an integral part of the hypothalamic developmental program that ensures the correct timing for glial phenotypes' generation. Importantly, we propose that the Klf10-/- mouse model represents a valuable tool for investigating the impact of reduced astrocyte and microglia populations in the homeostasis of the adult hypothalamus.

Immunological assessments indicated a higher presence of immune checkpoints and immune cells in cluster B, suggesting a greater likelihood of responsiveness to ICIs. The findings of this study highlight the potential of the TGF-β signaling pathway for prognostic classification and the development of personalized treatment strategies for BC patients, thereby enhancing our understanding of its significance in BC prognosis.

FXYD6 depletion counteracted KLF10 upregulation-triggered reduction in GC cell proliferation and elevation in apoptosis. In conclusion, KLF10 activates FXYD6 transcription, thereby impeding GC cell proliferation and promoting cell apoptosis.

Gla regulates the expression levels of DUSP5, ZFP36, KLF10, NR4A1, and RMI2 to against HCC, providing valuable insights for the application of Gla in HCC treatment.

Drug sensitivity analysis combining the GSE128099 showed a higher sensitivity to Gemcitabine in the low CAFs Score group (P = 0.0048). We speculate that these four CAFs-related genes are likely to be involved in regulating gemcitabine resistance in TNBC patients.

There is an elevated need to explore targets in cachexia, which will successfully translate into the clinic. Investigating a convergence point downstream of multiple signaling pathways might hold promise in developing effective therapies for cachexia.