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Lee, Wei-Ping
  • Associate Professor
  • Education: M.D. National Defense Medical Center ; Ph.D. University of Texas-Houston M.D Anderson Cancer Center
  • Office: 830R, The Chi Teh Bldg -The Medical Research Bldg,
  • Phone: 886-2-28712121#2672
  • Email:  這個 E-mail 地址已經被防止灌水惡意程式保護,您需要啟用 Java Script 才能觀看
Research--Molecular basis of gastric cancer and hepatoma
  • HBx and Akt: The X protein of hepatitis B virus (HBx) has been specifically implicated in the development of hepatocellular carcinoma (HCC). HBx has two roles in liver cells, namely pro-apoptotic and anti-apoptotic. Hepatitis B virus (HBV) containing Ser31-HBx is phosphorylated by Akt and associated with increased viral load and risks of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma.
  • Telomere and metronomic chemotherapy: Gemcitabine is an effective anti-cancer agent against solid tumors. The pharmacological mechanism of gemcitabine is known as incorporation into DNA and thereby inhibition of DNA synthesis. When used in metronomic chemotherapy of cancer, the agent may inhibit angiogenesis. It is still uncertain whether the agent can inhibit tumor growth by a mechanism other than DNA incorporation. In recent study, we show that gemcitabine causes telomere shortening by stabilizing TRF2 that is required for XPF-dependent telomere loss. Overexpression of TRF2 in the absence of gemcitabine also causes telomere shortening with simultaneous association of TRF2 with XPF/ERCC1.
  • Classical tumor biology: The p53 protein is a cell cycle regulator. When the cell cycle progresses, p53 plays an important role in putting a brake on the G1 phase to prevent unwanted errors during cell division. Akt is a downstream kinase of receptor tyrosine kinase. Upon activation, Akt phorphorylates IKK that then phosphorylates IκB and releases NF-κB, leading to transcriptional activation of Dmp1. Dmp1 is a transcriptional activator of Arf. It has been known that oncogene activation stabilizes p53 through transcriptional activation of Arf, which then binds and inhibits Mdm2. In recent study, we show that myc-associated zinc finger protein (MAZ) is a transcriptional repressor of the p53 promoter. Akt phosphorylates MAZ at Thr385, and the phosphorylated MAZ is released from the p53 promoter, leading to transcriptional activation of p53.
  • *Lee WP, Lan KH, Li CP, Chao Y, Lin HC, Lee SD. Akt phosphorylates myc-associated zinc finger protein (MAZ), releases P-MAZ from the p53 promoter, and activates p53 transcription. Cancer Letters. 2016; 375:9-19.


  • *Lee WP, Lan KH, Li CP, Chao Y, Lin HC, Lee SD. Oncogenic circuit constituted by Ser31-HBx and Akt increases risks of chronic hepatitis and hepatocellular carcinoma. BBA-Molecular Basis of Disease. 2016;1862:837-49.



  • *Lee WP, Lan KH, Li CP, Chao Y, Lin HC, Lee SD. Pro-apoptotic or anti-apoptotic property of X protein of hepatitis B virus is determined by phosphorylation at Ser31 by Akt. Arch Biochem Biophys. 2012;528:156-62.


  • Su CH, Chu WC, Lan KH, Li CP, Chao Y, Lin HC, Lee SD, Tsai YC, *Lee WP. Gemcitabine causes telomere attrition by stabilizing TRF2. European Journal of Cancer, 2012;48:3465-74.


Co-author papers






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