KLF8 (Kruppel Like Factor 8)

The studied meth-ctDNA markers are promising for the minimally-invasive detection and prognostication of CRPC but do not allow for clinical characterization of hsPC. Prospective studies are warranted for their use in therapy response and outcome prediction in CRPC and potential incremental value for PCa monitoring in PSA-low settings.

CircSEC24A silencing inhibited NSCLC cell malignancy through the miR-1253/KLF8 pathway, providing a potential therapeutic target for NSCLC.

This nomogram may be useful for a more accurate selection of patients for active surveillance protocols. Nonetheless, validation in a larger, multicentric, set of diagnostic PCa biopsies is mandatory for further confirmation of these results.

Our systematic study of generative methods showed that KLF8-DM produces the highest quality images with negligible image memorization. The higher classifier performance in the generatively augmented dataset suggests that this augmentation technique can be employed to enhance histopathology classifiers for various tasks.

Understanding the intricate molecular mechanisms underlying the metabolic reprogramming driven by KLF8 in lung cancer provides valuable insights into potential therapeutic strategies targeting the PPP. This study emphasizes the significance of KLF8 as a key modulator of metabolic pathways and indicates the potential of targeting the KLF8-G6PD axis for lung cancer treatment.

Klfs are associated with diseases such as carcinogenesis, oxidative stress, diabetes, liver fibrosis, thalassemia, and the metabolic syndrome. The aim of this review is to provide information about the relationship of Klfs with some diseases and physiological events and to guide future studies.

The stability of circ-ILF2 was also confirmed using RNase R and actinomycin D assays. In addition, tumour-associated macrophages (TAM) play important roles in cancer progressions, our results showed that circ-ILF2 in OSCC cells induced the M2 polarization of macrophages which provided new thoughts on immunotherapy. Our results suggest that circ-ILF2 may represent a potential therapeutic target in CDDP-resistant OSCC.

KLF8 levels are associated with chemoresistance in triple negative breast cancer patients and overexpression in breast cancer cells increased paclitaxel resistance. KLF8 and OGT co-regulate each other to form a feed-forward loop to promote CSCs phenotype and mammosphere formation of breast cancer cells. These results suggest a critical role of KLF8 and OGT in promoting CSCs and cancer progression, that may serve as potential targets for developing strategy to target CSCs specifically.

We have discovered that the prognosis-related lncRNAs/circRNAs-miRNA-mRNA network plays a significant role in the pathogenesis of HCC. These findings may offer fresh perspectives for further research into the pathogenesis of HCC and the search for novel treatments for HCC.

Introduction The drug-resistant mechanisms of the first-generation Bruton's tyrosine kinase (BTK) inhibitor, ibrutinib, has been extensively explored in chronic lymphocytic leukemia (CLL) patients. Integrated multi-omics were performed in our zanubrutinib-resistant CLL patients cohort. Due to spatial heterogeneity and clonal evolution among patients, deep targeted-gene NGS and ddPCR should be used complementarily to evaluate the emergence of resistant clones. BTK Cys481 and Leu528 were two main BTK resistant mutations in zanubrutinib resistant CLL patients.

Using promoter-luciferase reporter assays, we defined that upon TGF-β1 activation, phosphorylated Smad2 binds and promotes the KLF8 promoter activity, and knockdown of Smad2 inhibits KLF8 promoter activation. Together, these results demonstrate that TGF-β1 activates KLF8 expression by the Smad2 pathway, and KLF8 contributes to OC progression and may serve as a potential therapeutic strategy for treating OC patients.