3篇
您的检索式：作者名="Mingxi Gan"
|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Phosphorylation of glutaminase by PKCε is essential for its enzymatic activity and critically contributes to tumorigenesis显示文摘 | Tianyu Han Weihua Zhan Mingxi Gan Fanrong Liu Bentong Yu Y. Eugene Chin Jian-Bin Wang | 2018 | Cell Research2018，28，6： | 6 |
| 2 | USP14 regulates cell cycle progression through deubiquitinating CDK1 in breast cancer显示文摘Abnormal proliferation and cell cycle perturbation are the main hallmarks of breast cancer.Cyclin-dependent kinase 1(CDK1)is one of the key kinases for cell transition from the G2 phase to M phase during the cell cycle progression.However,little is known about the degradation mechanisms of CDK1.USP14(ubiquitin-specific processing protease 14)is an important proteasome-associated deubiquitinase that is critical for proteome homeostasis and plays a crucial role in the initiation and development of cancer.In this study,we find that USP14 shows high expression in breast cancer cells and results in the abnormal proliferation of cancer cells.Furthermore,we examine cell cycle distribution by flow cytometry and find that inhibition of USP14 causes cell cycle arrest in G2/M phase.As CDK1 is the key kinase in G2/M phase,we detect the interaction between USP14 and CDK1 and the effect of USP14 on the deubiquitination of CDK1.The results reveal that USP14 interacts with CDK1 and stabilizes CDK1 by deubiquitinating K48-linked ubiquitination.In conclusion,our findings reveal an indispensable role of USP14 in regulating cell cycle progression by stabilizing CDK1 in breast cancer,suggesting that USP14 may be used as a potential therapeutic target in breast cancer therapy. | Yuhan Liu Jing Xu Yanan Wang Mingxi Gan Qifan Hu Jianbin Wang Tianyu Han | 2022 | Acta Biochimica et Biophysica Sinica2022，54，11： | 0 |
| 3 | OXCT1 regulates NF-κB signaling pathway through β-hydroxybutyrate-mediated ketone body homeostasis in lung cancer显示文摘Metabolic reprogramming is one of the hallmarks of cancer.1 Ketone bodies behave as alternative fuel for cancer cells to support survival and proliferation.2 3-Oxoacid CoA-transferase 1 (OXCT1) is a key enzyme that catalyzes the first and rate-limiting step of ketolysis. Recently, several studies have revealed the significance of OXCT1 in cancer development, though the underlying mechanisms remain largely unknown.3 In this study, we revealed a novel regulatory mechanism for tumorigenesis that OXCT1 regulated SREBP1-TRIM21-p65 axis through ketone body homeostasis in non-small cell lung cancer (NSCLC). In terms of mechanism, we found that OXCT1 could activate NF-κB signaling pathway by suppressing transcriptional activity of the sterol regulatory element binding protein 1 (SREBP1). As a transcription factor, SREBP1 could bind to the promoter of E3 ubiquitin ligase TRIM21, which mediated the ubiquitination of p65. Furthermore, we demonstrated that OXCT1 could maintain the homeostasis of β-hydroxybutyrate (β-HB), which acted as a signaling metabolite to activate SREBP1. Thus, β-HB connected OXCT1 with SREBP1 to activate NF-κB signaling pathway and promoted tumor initiation and progression. Taken together, these findings highlight a previously unappreciated mechanism for activation of NF-κB signaling by OXCT1 and ketone body, and demonstrate that targeting OXCT1 can inhibit NSCLC tumorigenesis. | Zhuo Lu Tianyu Han Tao Wang Mingxi Gan Caifeng Xie Bentong Yu Jian-Bin Wang | 2023 | Genes & Diseases2023，10，2： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员