I received my Ph.D. in Basic Medical Sciences from National Cheng Kung University (2007–2013), following an M.S. in Biomedical Sciences from National Sun Yat-sen University (2004–2006) and a B.S. in Medical Technology from Kaohsiung Medical University (2000–2004). Professionally, I conducted postdoctoral training at the Department of Molecular and Cellular Biology, Baylor College of Medicine (March 2015–August 2019). Since August 2019, I have served as an Assistant Professor at the Graduate Institute of Medical Sciences, Taipei Medical University.

畢業於國立成功大學基礎醫學研究所，於 2007–2013 年取得博士學位；此前於 2004–2006 年就讀國立中山大學生物醫學研究所取得碩士學位，並於 2000–2004 年完成高雄醫學大學醫學技術學系學士訓練。研究經歷方面，我曾於 2015 年 3 月至 2019 年 8 月任職於美國貝勒醫學院分子及細胞生物學研究所擔任博士後研究員，並自 2019 年 8 月起於臺北醫學大學醫學科學研究所擔任助理教授。

本實驗室聚焦於膀胱癌惡性進展背後的「腫瘤微環境驅動機制」，以兩個最具可轉譯意義、且常在臨床樣本中共存的關鍵生態位為主軸：纖維母細胞活化所造成的膠原蛋白富集（COL-rich TME）與腫瘤代謝重編程（Warburg effect）衍生的乳酸富集微環境（lactate-rich TME）。我們整合細胞與分子生物學、3D 模型與功能性表型分析，系統性解析膠原蛋白訊號（如 DDR1/YAP 等）如何重塑癌細胞黏附、遷移與幹性，以及乳酸作為代謝訊息分子如何調控發炎與壓力反應路徑（如 STAT3 軸）、鐵恆定與治療反應；進一步探討兩種微環境之間的**互作與回饋（reciprocal crosstalk）**如何在化療/放療等治療壓力下驅動細胞可塑性、免疫抑制與抗藥性演化。最終目標是從「膠原—代謝—訊號」整合視角，鑑定可作為預後分層、生物標誌與治療標的的脆弱點，推進膀胱癌精準治療與轉譯應用。

Our laboratory investigates how the tumor microenvironment (TME) drives malignant progression and therapy resistance in bladder cancer, with a particular focus on two clinically prevalent and mechanistically intertwined niches: (i) a collagen-rich (COL-rich) stromal microenvironment generated by activated fibroblasts, and (ii) a lactate-rich metabolic microenvironment arising from tumor metabolic rewiring (the Warburg effect). By integrating molecular and cellular biology with functional phenotyping in 3D culture systems and clinically relevant models, we dissect how collagen-derived cues (e.g., DDR1/YAP signaling) reshape tumor cell adhesion, migration, and stem-like programs, and how lactate acts as a signaling metabolite to modulate stress/inflammatory pathways (e.g., STAT3), iron homeostasis, and therapeutic responses. A central theme of our work is the reciprocal crosstalk between lactate-rich and collagen-rich TMEs, and how this bidirectional interaction—especially under chemo-/radiotherapy-induced stress—fuels cellular plasticity, immune evasion, and the emergence of drug resistance. Ultimately, we aim to identify actionable vulnerabilities and biomarkers from a unified “matrix–metabolism–signaling” framework to advance translational strategies for precision treatment of bladder cancer.