Bio


Yunkyeong earned her PhD degree in February 2022. Her PhD work focused on the role of an epigenetic regulator in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) using a high-fat diet (HFD)-induced obese mice model. In addition, she studied the crosstalk between endoplasmic reticulum (ER) stress and autophagy. She joined in Dr. Anna L. Gloyn's Lab (Translational Genomics of Diabetes Lab) as a postdoctoral researcher from August 2022. She is involved in projects investigating molecular mechanisms for pancreatic islet-cell dysfunction in type 2 diabetes (T2D). Her research goal is to expand our knowledge about the molecular mechanisms of some metabolic diseases including T2D and explore therapeutic breakthrough.

Honors & Awards


  • Best Poster Award, The Korean Society for Integrative Biology (Dec 2021)
  • Keystone Symposia Scholarship, Keystone Symposia (Nov 2021)
  • Brain Korea 21 Scholarship, BK21 Plus (2017-2019)

Professional Education


  • Doctor of Philosophy, Sookmyung Women's University, Biological Sciences (2022)
  • Bachelor of Science, Sookmyung Women's University, Biological Sciences (2014)

Stanford Advisors


All Publications


  • Kazinol C from Broussonetia kazinoki stimulates autophagy via endoplasmic reticulum stress-mediated signaling ANIMAL CELLS AND SYSTEMS Lee, Y., Kwon, J., Jeong, J., Ryu, J., Kim, K. 2022; 26 (1): 28-36

    Abstract

    Autophagy modulators are considered putative therapeutic targets because of the role of autophagy in cancer progression. Kazinol C, a 1,3-diphenylpropane from the plant Broussonetia kazinoki, has been shown to induce apoptosis in colon cancer cells through the activation of AMPK at high concentrations. In the present study, we found that Kazinol C induced autophagy through endoplasmic reticulum stress-mediated unfolded protein response signaling in several normal and cancer cell lines at low concentrations of Kazinol C that did not induce apoptosis. Kazinol C activated the transducers of unfolded protein response signaling, leading to target gene expression, LC3-II conversion, and TFEB nuclear translocation. Chemical inhibition of endoplasmic reticulum stress reduced LC3-II conversion. In addition, blockade of autophagy by knockout of Atg5 or treatment with 3-MA enhanced Kazinol C-induced apoptosis. In summary, we have uncovered Kazinol C as a novel autophagy inducer and confirmed the role of autophagy as a cellular stress protector.

    View details for DOI 10.1080/19768354.2021.2023628

    View details for Web of Science ID 000741205000001

    View details for PubMedID 35308126

    View details for PubMedCentralID PMC8928802

  • Inhibition of autophagy sensitizes lignan-induced endoplasmic reticulum stress-mediated cell death BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS Kwon, J., Lee, Y., Jeong, J., Ryu, J., Kim, K. 2020; 526 (2): 300-305

    Abstract

    Relationship between autophagy and endoplasmic reticulum (ER) stress and their application to treat cancer have been actively studied these days. Recently, a lignan [(-)-(2R, 3R)-1,4-O-diferuloylsecoisolariciresinol, DFS] from Alnus japonica has been found to reduce the viability of colon cancer cells. In this study, we have observed DFS-induced autophagy in a variety of cancer cell lines. In addition, DFS led to ER stress, based on the activation of unfolded protein response (UPR) transducers and an elevated expression of UPR target genes in prostate and colon cancer cells. Further investigation has shown that DFS triggered the activation of AMP-activated protein kinase (AMPK) signaling and nuclear translocation of transcription factor EB (TFEB). Furthermore, the cytotoxicity of DFS was potentiated by the co-treatment of autophagy inhibitor in these cancer cells. This study has provided a noble implication that the combination of DFS and autophagy inhibition exerts a synergistic effect in cancer treatment.

    View details for DOI 10.1016/j.bbrc.2020.03.081

    View details for Web of Science ID 000530031800004

    View details for PubMedID 32209256