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2001年獲武漢大學學士學位，2007年獲中科院上海生科院健康科學研究所博士學位，2008至2013年在美國安德森癌癥中心(MD Anderson Cancer Center)做博士后研究，并成為奧德賽學者(Odyssey Fellow)。2013年8月起擔任中科院生物化學與細胞生物學研究所研究員，研究組長，博士生導師。

細胞代謝是維持生命活動的基礎生理過程，而腫瘤的發(fā)生、演進與代謝重塑（Metabolic Reprogramming）存在深刻的因果耦合關系。在致癌突變（如 KRAS、IDH、p53等）的驅(qū)動下，腫瘤細胞為應對微環(huán)境中營養(yǎng)匱乏、缺氧、氧化應激及免疫攻擊等選擇壓力，會系統(tǒng)性重編程糖酵解、三羧酸循環(huán)（TCA）、氨基酸及脂質(zhì)代謝通路。這種適應性改變不僅為細胞快速增殖提供生物能（ATP）及生物合成前體（核苷酸、脂質(zhì)、蛋白質(zhì)），還通過維持細胞內(nèi)氧化還原穩(wěn)態(tài)（Redox Homeostasis）以抵御凋亡信號。

值得注意的是，代謝重塑常伴隨特定代謝中間產(chǎn)物或“致癌代謝物”（Oncometabolites）的異常蓄積。例如，IDH1/2突變導致的 D-2-羥基戊二酸（D-2-HG）堆積，以及 FH或 SDH缺陷引起的琥珀酸、延胡索酸累積。這些代謝物可作為競爭性抑制劑干擾 α-酮戊二酸（α-KG）依賴性雙加氧酶（如 TET 家族 DNA 去甲基化酶、組蛋白去甲基化酶），引發(fā)廣泛的表觀遺傳重編程（Epigenetic Reprogramming），進而紊亂基因轉錄程序、阻滯細胞分化并促進惡性轉化；同時，它們亦可通過蛋白質(zhì)翻譯后修飾（如琥珀?；?、乳酸化）直接調(diào)控信號轉導網(wǎng)絡，介導治療抵抗與遠處轉移。

近年研究揭示，代謝產(chǎn)物并非局限于胞內(nèi)的被動參與者，而是具備主動分泌能力的信號分子。腫瘤細胞通過單羧酸轉運蛋白（MCTs）、溶質(zhì)載體（SLCs）等轉運系統(tǒng)將乳酸、支鏈α-酮酸（BCKAs）、氨、乙酸等代謝物釋放至腫瘤微環(huán)境（TME）。這些胞外代謝物構成了復雜的“代謝-免疫”通訊語言：它們可通過結合 G 蛋白偶聯(lián)受體（如 GPR81、SUCNR1、GPR34）或作為底物介導胞外蛋白質(zhì)翻譯后修飾（如胞外 CD44 乳酸化），誘導腫瘤相關巨噬細胞（TAMs）向 M2 型極化、抑制 CD8?T 細胞效應功能、促進調(diào)節(jié)性 T 細胞（Tregs）富集與活化，從而塑造免疫抑制性生態(tài)位并驅(qū)動免疫逃逸。

基于此，本實驗室聚焦于腫瘤代謝調(diào)控的分子機制與微環(huán)境互作網(wǎng)絡，致力于解析關鍵代謝酶及其產(chǎn)物在腫瘤發(fā)生、免疫逃逸及治療耐藥中的因果作用；旨在鑒定具有高靈敏度和特異性的代謝相關生物標志物（Biomarkers），并挖掘可干預的節(jié)點性代謝靶點，為癌癥的精準分型、代謝干預及聯(lián)合免疫治療提供堅實的科學依據(jù)與創(chuàng)新策略。

（*Corresponding author）

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