p52-ZER6/G6PD轴通过激活戊糖磷酸途径改变有氧糖酵解并促进肿瘤进展。

IF 5.9 2区 医学 Q1 ONCOLOGY
Yu Tang, Wenfang Li, Li Qiu, Xia Zhang, Lei Zhang, Makoto Miyagishi, Hezhao Zhao, Shourong Wu, Vivi Kasim
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引用次数: 2

摘要

糖代谢异常是肿瘤代谢重编程的一个亮点,与恶性肿瘤的发生发展密切相关。p52-ZER6是c2h2型锌指蛋白,促进细胞增殖和肿瘤发生。然而,其在调节生物和病理功能中的作用仍然知之甚少。在这里,我们研究了p52-ZER6在肿瘤细胞代谢重编程中的作用。具体来说,我们证明了p52-ZER6通过正向调节葡萄糖-6-磷酸脱氢酶(G6PD)的转录促进肿瘤糖代谢重编程,G6PD是戊糖磷酸途径(PPP)中的限速酶。通过激活PPP,我们发现p52-ZER6可以促进核苷酸和烟酰胺腺嘌呤二核苷酸磷酸的产生,从而为肿瘤细胞提供核糖核酸和细胞还原剂的构建块,用于清除活性氧,从而促进肿瘤细胞的增殖和活力。重要的是,p52-ZER6以p53独立的方式促进ppp介导的肿瘤发生。综上所述,这些发现揭示了p52-ZER6通过p53独立的过程调节G6PD转录的新作用,最终导致肿瘤细胞代谢重编程和肿瘤发生。我们的研究结果表明,p52-ZER6是诊断和治疗肿瘤和代谢紊乱的潜在靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The p52-ZER6/G6PD axis alters aerobic glycolysis and promotes tumor progression by activating the pentose phosphate pathway.

The p52-ZER6/G6PD axis alters aerobic glycolysis and promotes tumor progression by activating the pentose phosphate pathway.

The p52-ZER6/G6PD axis alters aerobic glycolysis and promotes tumor progression by activating the pentose phosphate pathway.

The p52-ZER6/G6PD axis alters aerobic glycolysis and promotes tumor progression by activating the pentose phosphate pathway.

Abnormal glucose metabolism is a highlight of tumor metabolic reprogramming and is closely related to the development of malignancies. p52-ZER6, a C2H2-type zinc finger protein, promotes cell proliferation and tumorigenesis. However, its role in the regulation of biological and pathological functions remains poorly understood. Here, we examined the role of p52-ZER6 in tumor cell metabolic reprogramming. Specifically, we demonstrated that p52-ZER6 promotes tumor glucose metabolic reprogramming by positively regulating the transcription of glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme in the pentose phosphate pathway (PPP). By activating the PPP, p52-ZER6 was found to enhance the production of nucleotides and nicotinamide adenine dinucleotide phosphate, thereby providing tumor cells with the building blocks of ribonucleic acids and cellular reductants for reactive oxygen species scavenging, which subsequently promotes tumor cell proliferation and viability. Importantly, p52-ZER6 promoted PPP-mediated tumorigenesis in a p53-independent manner. Taken together, these findings reveal a novel role for p52-ZER6 in regulating G6PD transcription via a p53-independent process, ultimately resulting in tumor cell metabolic reprogramming and tumorigenesis. Our results suggest that p52-ZER6 is a potential target for the diagnosis and treatment of tumors and metabolic disorders.

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来源期刊
Oncogenesis
Oncogenesis ONCOLOGY-
CiteScore
11.90
自引率
0.00%
发文量
70
审稿时长
26 weeks
期刊介绍: Oncogenesis is a peer-reviewed open access online journal that publishes full-length papers, reviews, and short communications exploring the molecular basis of cancer and related phenomena. It seeks to promote diverse and integrated areas of molecular biology, cell biology, oncology, and genetics.
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