Nanog promotes proliferation, migration, and invasion of gastric cancer cells via regulation of the KDM5B/H3K4me3 epigenetic axis

作者：Lili Ma, Lin Lu, Xiaohui Liu, Lei Wang, Yan Liu, Yaqi Wang, Yankun Liu, Jinghua Zhang, Yufeng Li · 发表于：Advances in Clinical and Experimental Medicine · 年份：2026 · DOI：10.17219/acem/211940 · 研究领域：Immune cells in cancer、Graphene and Nanomaterials Applications、Epigenetics and DNA Methylation

BACKGROUND: Nanog, a transcription factor, is involved in cancer initiation and progression. OBJECTIVES: To explore the potential regulatory mechanism of Nanog in gastric cancer. MATERIAL AND METHODS: Immunohistochemistry (IHC) was used to examine E-cadherin, N-cadherin, Nanog, and KDM5B in gastric cancer (Ca), metastatic lymph node cancer (L), and adjacent normal tissues (N). MTT, migration, and invasion assays were used to evaluate cell viability, migration, and invasion of gastric cancer cells SGC-7901 induced by transforming growth factor (TGF)-β1, or with Nanog overexpression/knockdown. Western blot was used to examine the relative protein expression of E-cadherin, N-cadherin, Nanog, and lysine-specific demethylase 5B (KDM5B) in cells. KDM5B was silenced by siRNA in cells, and E-cadherin, N-cadherin, and H3K4me3 were examined with western blot, while the interaction between Nanog and KDM5B was examined using a co-immunoprecipitation (Co-IP) assay. Furthermore, H3K4me3 protein expression was validated in N, Ca, and L tissues using IHC. RESULTS: E-cadherin was hypoexpressed, while N-cadherin, Nanog, and KDM5B were hyperexpressed in the Ca and L groups compared with the N group. TGF-β1 and Nanog enhanced cell viability, migration, and invasion by promoting epithelial-mesenchymal transition (EMT). KDM5B was identified to bind to Nanog and was positively regulated by Nanog, and functioned as a negative regulator of histone H3 Lys4 trimethylation (H3K4me3) in SGC-7901 cells. K...