KLF14 (KLF Transcription Factor 14)

In addition, we assessed the effect of gene polymorphisms on the course of the disease, and rapid disease progression was found to be correlated with the presence of these polymorphisms. These findings could help determine the risk of developing MPNs and patient prognosis.

Moreover, a deeper understanding of the molecular regulatory mechanisms and disease associations of KLF14 could inform the development of targeted therapies and personalized medicine strategies. Thus, the current study underscores the significance of KLF14 as a trans-regulatory gene and a potential therapeutic target, emphasizing its intricate role in biological regulation and disease pathogenesis.

These results demonstrate genkwanin's therapeutic potential in triple-negative breast cancer and its effect on targeting metastasis.

This study highlights that FOSL1 is negatively regulated by KLF14 in glioblastoma and suggests that KLF14 overexpression can mitigate tumor growth by inhibiting FOSL1, thus identifying KLF14 as a novel molecular target for treating glioblastoma. Further research into the interplay and regulatory dynamics between KLF14 and FOSL1 under varying stress conditions can enhance the precision of glioblastoma treatment.

Our findings not only establish EZH2 as a biomarker for MM prognosis but also highlight the EZH2-KLF14-SLC7A11 axis as a potential target for MM treatment.

Our data revealed a previously unidentified function of KLF14 in promoting ferroptosis, which results in the suppression of cell proliferation. Mechanistically, we revealed a novel regulatory mechanism by which KLF14 targets GPX4. These findings suggest a novel strategy to induce ferroptosis through the targeting of KLF14 in human cervical cancer cells.

Furthermore, EPHA4, a shared downstream target gene of KLF14 and EGR2, altered tumor sensitivity to MEK inhibitor treatment. Altogether, patient-derived CRC cells undergo both common and distinct chromatin remodeling in PDO and PDX/PDOX, driven largely by their respective microenvironments, which results in differences in growth and drug sensitivity and needs to be taken into consideration when interpreting their ability to predict clinical outcome.

KLF14 also activated the JNK pathway to induce S-phase arrest and promote the expression of CDK2 and CCNA2. In summary, KLF14 activates the JNK-signaling pathway to induce S-phase arrest in cervical cancer cells.

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.

We measured the KLF14 ubiquitination level and KLF14 enrichment on the VEPH1 promoter after MG132 treatment...Inhibiting KLF14 or VEPH1 partially minimized the inhibitory effect of WWP1 silencing on liver cancer cell proliferation and invasion/migration. In summary, WWP1 degrades KLF14 through ubiquitination, hence repressing VEPH1 expression and accelerating proliferation and invasion/migration of liver cancer cells.

The result subsequently confirmed the KLF14/miR-1283 signaling suppressed cell proliferation in HER2+ breast cancer. Our results suggested that the KLF14/miR-1283/TFAP2C axis inhibited HER2+ breast cancer progression, which might provide novel insight into mechanical exploration for this disease.