PFKP可能通过增强c-Myc表达促进HNSCC进展、生长和转移。为了进一步探究c-Myc调控PFKP转录的机制,通过生物信息学、TCGA-HNSCC数据及K-M生存分析揭示,转录因子c-Myc与PFKP呈正相关。来自公共数据库的ChIP-seq和RNA-seq数据显示,c-Myc在PFKP的启动子区域具有显信号,并且淋巴瘤细胞中c-Myc减少后PFKP mRNA水平表达量显著...
在PFKP敲低的细胞中过表达c-Myc,结果显示,过表达c-Myc逆转了PFKP敲低对于细胞增殖、血管生成、迁移和侵袭的抑制作用。PFKP可能通过增强c-Myc表达促进HNSCC进展、生长和转移。为了进一步探究c-Myc调控PFKP转录的机制,通过生物信息学、TCGA-HNSCC数据及K-M生存分析揭示,转录因子c-Myc与PFKP呈正相关。来自公共数据库的C...
Mechanistically, PFKP increases the ERK-mediated stability of c-Myc, thereby driving progression of HNSCC. Moreover, c-Myc stimulates PFKP expression at the transcriptional level, thus forming a positive feedback loop between PFKP and c-Myc. Additionally, our multiple models demonstrate that co-...
NM002627-8 pcDNA3.1/MycHisA 全长 C-His、C-Myc 哺乳细胞 2800 NM002627-9 pCMV-Tag 2A 全长 N-Flag 哺乳细胞 2800 NM002627-10 pCMV-Tag 4A 全长 C-Flag 哺乳细胞 2800 NM002627-11 pCMV-HA 全长 N-HA 哺乳细胞 2800 NM002627-12 pEGFP-C1 全长 N-EGFP 哺乳细胞 2800 NM002627-13 pEGFP-N1 ...
Jiang L, Qi X, Lai M, Zhou J, Yuan M, You J, Liu Q, Pan J, Zhao L, Ying M, Ji J, Li K, Zhang Y, Pan W, He Q, Yang B, Cao J (2024) WDR20 prevents hepatocellular carcinoma senescence by orchestrating the simultaneous USP12/46-mediated deubiquitination of c-Myc. Proc Natl...
图2 PFKP促进了ERK介导的c-Myc的稳定性 (图源:Liu, Weiwei et al., Mol Cancer., 2024) 3.c-Myc促进HNSCC中PFKP的转录 在PFKP敲低的细胞中过表达c-Myc,结果显示,过表达c-Myc逆转了PFKP敲低对于细胞增殖、血管生成、迁移和侵袭的抑制作用。PFKP可能通过增强c-Myc表达促进HNSCC进展、生长和转移。为了进一步探...
Protein levels of PFKP, beta-catenin, and c-Myc were examined using western blot analysis. The results showed that knockdown of HOTAIRM1 enhanced Ara-C-induced reduction of cell viability and increase of cell apoptosis. HOTAIRM1 knockdown suppressed the glucose consumption and lactate production, ...
Protein levels of PFKP, β-catenin, and c-Myc were examined using western blot analysis. The results showed that knockdown of HOTAIRM1 enhanced Ara-C-induced reduction of cell viability and increase of cell apoptosis. HOTAIRM1 knockdown suppressed the glucose consumption and lactate production, ...