NCKU-Department of Pharmacology

Welcome to NCKU-Department of Pharmacology

Cheung, Chun Hei Antonio

 N A M E / T I T L E
 ( Cheung, Chun Hei Antonio, Ph.D., MRSNZ )
 T E L
 886-6 235-3535 ext 5503
 F A X
 886-6 274-9296
 E - M A I L
  Ph.D, Molecular Medicine, The University of Auckland, New Zealand
  B.Tech with First Class Honours, Biomedical science, The University of Auckland,  New Zealand

Tamoxifen is a hormone modulator that has been widely used as an anti-cancer agent. Typically, patients with estrogen receptor positive (ER-positive) breast tumors will receive Tamoxifen either as a first line treatment or as a second line treatment after surgery. Despite the benefit of using Tamoxifen as hormonal therapy in treating ER-positive breast cancers has been widely demonstrated in patients at early treatment stages, its effectiveness seems to be significantly reduced in patients after five years post-treatment. Interestingly, two thirds of the tumors that become resistant to Tamoxifen continue to express ER. Thus, it is necessary to develop novel strategies that can be applied to target both ER-positive Tamoxifen-resistant and estrogen-independent breast cancer cells


Investigations on the possibility of using Survivin inhibitors for the treatment of Tamoxifen-resistant or estrogen-independent breast cancers


2011 - NHRI Research Day “Elected paper” award

2010 - American Association for Cancer Research Scholar-in-training award finalist

2010 - The 15 th Taiwan Joint Cancer Conference “Outstanding research poster” award

2010 - NHRI Research Day “Excellent research poster” award

2009 - NHRI Research Day “Elected thesis” award

2009 - The University of Auckland International Doctoral Scholar

2006 - The Maurice & Phyllis Paykel Trust Post-graduate travel award
Huang WT, Tsai YH, Chen SH, Kuo CW, Kuo YL, Lee KT, Chen WC, Wu PC, Chuang CY, Cheng SM, Lin C-H, Leung EY, Chang YC and Cheung CHA*; HDAC2 and HDAC5 up-regulations modulate survivin and miR-125a-5p expressions and promotes hormone therapy resistance in estrogen receptor positive breast cancer cells; Frontiers in Pharmacology. (2017) 8:902 [Ranking: Pharmacology & Pharmacy 33/256, top 12.9%]

Lee JYC, Kuo CW, Tsai SL, Cheng SM, Chen SH, Chan HH, Lin CH, Li CF, Kanwar, JR, Leung EY, Cheung CCH, Huang WJ, Wang YC and Cheung CHA*; Inhibition of HDAC3- and HDCA6-promoted survivin expression plays an important role in SAHA-induced autophagy and viability reduction in breast cancer cells; Frontiers in Pharmacology. (2016) 7:81 [Ranking: Pharmacology & Pharmacy 33/256, top 12.9%]

 Solicited Editorial: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition); Autophagy (2016) 12(1):1-222 [Ranking: Cell Biology 22/189, top 11.6%]
 Sarvagalla S, Cheung CHA, Tsai JY and Coumar MS*; Disruption of protein-protein interaction: Hot Spot detection, structure-based virtual screening and in vitro testing for anti-cancer drug target-survivin; RSC Advances (2016) 6:31947-41959 [Ranking: Chemistry / Multidisciplinary 59/166, top 35.5%]
 Cheng SM, Chang YC, Liu CY, Lee JYC, Chen HH, Kuo CW, Lin KY, Tsai SL, Chen SH, Li CF, Leung E, Kanwar JR, Huang CC, Chang JY and Cheung CHA*; YM155 down-regulates survivin and XIAP, modulates autophagy and induces autophagy-dependent DNA damage in breast cancer cells; British Journal of Pharmacology (2015) 172(1):214-24 [Ranking: Pharmacology & Pharmacy 19/256, top 7.4%]
 Coumar MS, Tsai FY, Kanwar JR, Sarvagalla S and Cheung CHA*; Treat cancer by targeting survivin: just a dream or future reality? (invited review); Cancer Treatment Reviews (2013) 39:802-811 [Ranking: Oncology 16/217, top 7.4%]
Huang CC, Chen KL, Cheung CHA, and Chang JY*; Autophagy induced by cathepsin S inhibition induces early ROS production, oxidative DNA damage, and cell death via xanthine oxidase; Free Radical Biology and Medicine (2013) 65:1473-1486 [Ranking: Endocrinology & Metabolism 17/138, top 12.3%]
 Chen KL, Chang WS, Cheung CHA, Lin CC, Huang CC, Yang YN, Kuo CP, Kuo CC, Chang YH, Lin KJ, Wu CM and Chang JY*; Targeting cathepsin S induces tumor cell autophagy via the EGFR-ERK signaling pathway; Cancer Letters (2012) 317(1):89-98 [Ranking: Oncology 25/217, top 11.5%]
 Cheung CHA, Chen HH, Cheng LT, Lyu KW, Kanwar JR and Chang JY*; Targeting Hsp90 with small molecule inhibitors induces the over-expression of the anti-apoptotic molecule, survivin, in human A549, HONE-1 and HT-29 cancer cells; Molecular Cancer (2010) 9:77 Ranked as "Highly Accessed" by BMC & selected as "Key scientific journal article" by Lead Discovery [Ranking: Biochemistry & Molecular Biology 36/286, top 12.6%]
 Cheung CHA, Chen HH, Kuo CC, Chang CY, Coumar MS, Hsieh HP and Chang JY*; Survivin counteracts the therapeutic effect of microtubule de-stabilizers by stabilizing tubulin polymers; Molecular Cancer (2009) 8:43 Ranked as "Highly Accessed" by BMC; listed as "Featured news" in NewsRx - Cancer [Ranking: Biochemistry & Molecular Biology 36/286, top 12.6%] 
 BooK Chapter: Caspase-independent Apoptosis: Encyclopedia of Cancer (2015) Springer Reference edited by Manfred Schwab, Chapter 7072-1


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