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KMT2A maintains stemness of gastric cancer cells through regulating Wnt/β-catenin signaling-activated transcriptional factor KLF11

The molecular mechanisms of epigenetic regulation in gastric cancer development are not yet well established. In this study, we demonstrated that KMT2A was highly expressed in gastric cancer and associated with poor outcomes of patients and revealed that KMT2A was significantly associated with stemn...

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Detalles Bibliográficos
Autores principales: Deng, Chongwen, Ye, Chunhua, Liao, Xiwang, Zhou, Fuyin, Shi, Youxiong, Zhong, Hong, Huang, Junbiao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: De Gruyter 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10655684/
https://www.ncbi.nlm.nih.gov/pubmed/38025523
http://dx.doi.org/10.1515/med-2023-0764
Descripción
Sumario:The molecular mechanisms of epigenetic regulation in gastric cancer development are not yet well established. In this study, we demonstrated that KMT2A was highly expressed in gastric cancer and associated with poor outcomes of patients and revealed that KMT2A was significantly associated with stemness and increased nuclear β-catenin in gastric cancer. Mechanistically, KMT2A activated the translocation of β-catenin into the nucleus of gastric cancer cells, and then, β-catenin served as a coactivator of KLF11, which promoted the expression of specific gastric cancer stemness-related molecules, including SOX2 and FOXM1. Together, KMT2A is an important epigenetic regulator of gastric cancer stemness, which provides a novel insight to the potential application of targeting against KMT2A in treating gastric cancer.