课题组获得中组部“***计划”和国家基金委“优秀青年基金”,重点等项目的资助。实验室目前的主要研究方向是肿瘤代谢，包括肿瘤细胞（特别是p53缺陷和突变肿瘤细胞）中代谢异常发生的分子和调控机制，以及细胞（肿瘤细胞及免疫细胞）感知微环境中营养物质改变的分子机制和生理功能。部分研究成果发表于Nature（2013，2019），Nature Cell Biology（2011,2013， 2021）, PNAS （2021） 和Nature Communications（2018，2020）等杂志上。
Metabolic reprogramming is ultimately associated with genetic mutations, transcription and signaling transduction changes. Among the genes that are critical for tumour development, p53 is the most frequently mutated gene in human cancer. Although p53 has been reported to regulate various biological events, it is still challenging in treating patients with p53 deficient or mutant tumours, and what confers p53 deficient and mutant tumour cells proliferative and/or survival advantages require further investigation.
Emerging evidence suggest that metabolic regulation is central for p53-mediated tumour suppression. To study this, we have found that NADPH metabolism and its associated central carbon metabolism are markedly reprogrammed in many tumour cells induced by p53 inactivation (Nature 2013, Nature Cell Biology 2011, 2013). And also, tumour cells with p53 mutations or depletion unexpectedly display aberrant ammonia metabolism and polyamine biosynthesis (Nature, 2019). Moreover, p53 has a role in controlling asparagine/aspartate homeostasis dictating cell fate decisions (Nature Communications, 2020). Currently, we are interested in how p53 and its mutants directly sense metabolic changes, understanding these issues which we believe will increase our knowledge of the physiological and pathological functions of p53, and may provide new mechanistic insights into tumors harboring p53 mutation(s) or loss. Today, I will discuss with you what we have and what we have learned about p53 and cancer metabolism.
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