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- 저자 : Ren Yongxia (검색결과 2 건)
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Zhao Jingyi,Li Bingyan,Ren Yongxia,Liang Tiansong,Wang Juan,Zhai Suna,Zhang Xiqian,Zhou Pengcheng,Zhang Xiangxian,Pan Yuanyuan,Gao Fangfang,Zhang Sulan,Li Liming,Yang Yongqiang,Deng Xiaoyu,Li Xiaole,C 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-
Compelling evidence has indicated the vital role of lysine-specific demethylase 4 A (KDM4A), hypoxia-inducible factor-1α (HIF1α) and the mechanistic target of rapamycin (mTOR) signaling pathway in nasopharyngeal carcinoma (NPC). Therefore, we aimed to investigate whether KDM4A affects NPC progression by regulating the HIF1α/DDIT4/mTOR signaling pathway. First, NPC and adjacent tissue samples were collected, and KDM4A protein expression was examined by immunohistochemistry. Then, the interactions among KDM4A, HIF1α and DDIT4 were assessed. Gain- and loss-of-function approaches were used to alter KDM4A, HIF1α and DDIT4 expression in NPC cells. The mechanism of KDM4A in NPC was evaluated both in vivo and in vitro via RT-qPCR, Western blot analysis, MTT assay, Transwell assay, flow cytometry and tumor formation experiments. KDM4A, HIF1α, and DDIT4 were highly expressed in NPC tissues and cells. Mechanistically, KDM4A inhibited the enrichment of histone H3 lysine 9 trimethylation (H3K9me3) in the HIF1α promoter region and thus inhibited the methylation of HIF1α to promote HIF1α expression, thus upregulating DDIT4 and activating the mTOR signaling pathway. Overexpression of KDM4A, HIF1α, or DDIT4 or activation of the mTOR signaling pathway promoted SUNE1 cell proliferation, migration, and invasion but inhibited apoptosis. KDM4A silencing blocked the mTOR signaling pathway by inhibiting the HIF1α/DDIT4 axis to inhibit the growth of SUNE1 cells in vivo. Collectively, KDM4A silencing could inhibit NPC progression by blocking the activation of the HIF1α/DDIT4/mTOR signaling pathway by increasing H3K9me3, highlighting a promising therapeutic target for NPC.
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miR-29 family inhibited the proliferation and migration of lung cancer cells by targeting SREBP-1
Lin Lin,Bao Yongxia,Tian Miao,Ren Qiu,Zhang Wei 대한독성 유전단백체 학회 2022 Molecular & cellular toxicology Vol.18 No.2
Backgrounds Lipid metabolism dysregulation is an important characteristic of tumor cells. Increased lipid metabolism provides a vital material and energy source for tumor growth, thereby promoting tumor invasion and metastasis. Objectives In the current work, we carried out a series of in vivo and in vitro studies to explore the relationship between miR-29 and lung cancer. Results The results showed that miR-29 was down-regulated in lung cancer, and overexpression of miR-29 inhibited the proliferation and migration of lung cancer cells (in vitro). Anti-lung cancer effect of miR-29 in vivo was evaluated, and results indicated that transfection of miR-29b/c markedly inhibited lung tumor growth (in vivo). We further explored the potential mechanism by which miR-29 could inhibit the cell proliferation of lung cancer. It is well known that lipid metabolism dysregulation is an important characteristic of tumor cells. Increased lipid metabolism provides a vital material and energy source for tumor growth, thereby promoting tumor invasion and metastasis, and sterol regulatory element-binding protein 1 (SREBP) is involved in liposome metabolism. Therefore, we analyzed the interaction between miR-29C and SREBP-1 in lung cancer cells. Bioinformatics analysis showed that the miR-29 has the potential binding site on SCAP and SREBP mRNA, and Luciferase reporter gene assays revealed the interaction between 3′UTR of SREBP-1 mRNA and miR-29c. Further study showed that miR-29 suppressed (SREBP-1) expression by interacting with 3′UTR of SREBP-1. Further work indicated that miR-29 transfection strongly inhibited lung cancer cell proliferation, which was rescued by the overexpression of SREBP-1. Conclusion These fi ndings demonstrate that transfection of miR-29 suppressed lung cancer proliferation via inhibiting SREBP-1 expression. The current study provides a basis for exploring the targeted agents against lung cancer.
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