Kang Yell Choi


Affiliation: Yonsei University
Country: Korea


  1. Ryu W, Lee J, Cho Y, Lee G, Seo M, Lee S, et al. A Therapeutic Strategy for Chemotherapy-Resistant Gastric Cancer via Destabilization of Both β-Catenin and RAS. Cancers (Basel). 2019;11: pubmed publisher
    ..Overall, the small-molecule approach degrading both β-catenin and RAS has potential as a therapeutic strategy for treating GC patients resistant to current standard chemotherapies. ..
  2. Choi S, Kim H, Cha P, Seo S, Lee C, Choi Y, et al. CXXC5 mediates growth plate senescence and is a target for enhancement of longitudinal bone growth. Life Sci Alliance. 2019;2: pubmed publisher
    ..Collectively, our findings reveal an important role for CXXC5 as a suppressor of longitudinal bone growth involving growth plate activity. ..
  3. Jeong W, Park J, Kim W, Ro E, Jeon S, Lee S, et al. WDR76 is a RAS binding protein that functions as a tumor suppressor via RAS degradation. Nat Commun. 2019;10:295 pubmed publisher
    ..The clinical relevance of RAS regulation by WDR76 is indicated by the inverse correlation of their expressions in HCC tissues. Our study demonstrates that WDR76 functions as a tumor suppressor via RAS degradation. ..
  4. Park J, Cho Y, Shin W, Lee S, Lee J, Kim T, et al. A Ras destabilizer KYA1797K overcomes the resistance of EGFR tyrosine kinase inhibitor in KRAS-mutated non-small cell lung cancer. Sci Rep. 2019;9:648 pubmed publisher
    ..The destabilization of Ras via inhibition of the Wnt/β-catenin pathway is a potential therapeutic strategy for KRAS-mutated NSCLC that is resistant to EGFR TKI. ..
  5. Lee S, Jeong W, Cho Y, Cha P, Yoon J, Ro E, et al. β-Catenin-RAS interaction serves as a molecular switch for RAS degradation via GSK3β. EMBO Rep. 2018;19: pubmed publisher
  6. Lee S, Cho Y, Cha P, Yoon J, Ro E, Jeong W, et al. A small molecule approach to degrade RAS with EGFR repression is a potential therapy for KRAS mutation-driven colorectal cancer resistance to cetuximab. Exp Mol Med. 2018;50:153 pubmed publisher
  7. Zahoor M, Cha P, Choi K. Indirubin-3'-oxime, an activator of Wnt/?-catenin signaling, enhances osteogenic commitment of ST2 cells and restores bone loss in high-fat diet-induced obese male mice. Bone. 2014;65:60-8 pubmed publisher
    ..Overall, our results indicate that I3O could be a potential therapeutic agent for obese male patients through downregulation of abdominal fat and net increment in trabecular bone density. ..
  8. Shin W, Lee S, Hwang J, Park J, Cho Y, Ro E, et al. Identification of Ras-degrading small molecules that inhibit the transformation of colorectal cancer cells independent of β-catenin signaling. Exp Mol Med. 2018;50:71 pubmed publisher
    ..Small molecules that degrade Ras independent of β-catenin may able to be used in treatments for cancers caused by aberrant EGFR and Ras. ..
  9. Kim H, Choi S, Yoon J, Lim H, Lee H, Choi J, et al. Small molecule inhibitors of the Dishevelled-CXXC5 interaction are new drug candidates for bone anabolic osteoporosis therapy. EMBO Mol Med. 2016;8:375-87 pubmed publisher
    ..In conclusion, small-molecule inhibitors of the Dvl-CXXC5 interaction that block negative feedback regulation of Wnt/β-catenin signaling are potential candidates for the development of bone anabolic anti-osteoporosis drugs. ..

More Information


  1. Lee S, Hwang J, Choi K. Interaction of the Wnt/?-catenin and RAS-ERK pathways involving co-stabilization of both ?-catenin and RAS plays important roles in the colorectal tumorigenesis. Adv Biol Regul. 2018;68:46-54 pubmed publisher
    ..Overall, the increments of ?-catenin and RAS especially mutant KRAS by APC loss play important roles in the cooperative tumorigenesis of CRC. ..
  2. Kim H, Yang D, Shin S, Kim M, Yoon J, Kim S, et al. CXXC5 is a transcriptional activator of Flk-1 and mediates bone morphogenic protein-induced endothelial cell differentiation and vessel formation. FASEB J. 2014;28:615-26 pubmed publisher
    ..Overall, CXXC5 is a transcriptional activator for Flk-1, mediating BMP signaling for differentiation and migration of endothelial cell and vessel formation. ..
  3. Lee S, Kim M, Kim H, Lee Y, Kim H, Nam K, et al. The Dishevelled-binding protein CXXC5 negatively regulates cutaneous wound healing. J Exp Med. 2015;212:1061-80 pubmed publisher
    ..Together, these data suggest that CXXC5 would represent a potential target for future therapies aimed at improving wound healing. ..
  4. Park J, Jeong W, Kim M, Min D, Choi K. Retinoic-acid-mediated HRas stabilization induces neuronal differentiation of neural stem cells during brain development. J Cell Sci. 2016;129:2997-3007 pubmed publisher
    ..In summary, this study shows that retinoic acid stabilizes HRas protein during neurogenesis, and that this is required for NSC differentiation into neurons and murine brain development. ..
  5. Lee S, Seo S, Lee D, Pi L, Lee W, Choi K. Targeting of CXXC5 by a Competing Peptide Stimulates Hair Regrowth and Wound-Induced Hair Neogenesis. J Invest Dermatol. 2017;137:2260-2269 pubmed publisher
    ..Overall, these findings suggest that the CXXC5-Dishevelled interaction is a potential target for the treatment of hair loss. ..