What We Work On

What We Work On

  1. Hepatocellular Carcinoma  

Most hepatocellular carcinoma (HCC) arises in the background of chronic hepatitis/cirrhosis and usually follow a multistep sequence.  It takes approximately 10-30 years from chronic hepatitis and 3-5 years from precancerous lesions (dyaplstic foci/dysplastic nodules) to become HCC. Therefore, if we were able to diagnose or prevent precancerous lesions or early stage HCC, we would be able to expect improved survival and prognosis.  Thus, it is very important to understand the “molecular signature“ of precancerous lesions or early stage HCC.

  2. Hepatic cancer stem cells  

Cancer stem cells have the ability to self-renew, differentiate, and proliferate, have greater tumorigenicity and chemoresistance, and are associated with poor prognosis. Cancer stem cells have been recently highlighted in cancer research because cancer stem cell targeted therapy could be a novel treatment method that prevents the metastasis and recurrence of cancers.  Also, an assay of stemness-related marker expression in cancerous tissues might be a simple and very important test for prognosis and designing a custom treatment plan.

  3. Hepatic cancer stem cells and tumor microenvironment  

Tumor behavior and therapeutic response depend on not only cancer cells themselves, but also on the microenvironment surrounding the cancer cells. Tumor microenvironment is genetically more stable compared to cancer cells that it might be a novel therapeutic target. Therefore, understanding the relationship between hepatic cancer stem cells and their microenvironment might be a clue to accurate prediction of prognosis and efficient therapeutic strategy.


The main research theme of our lab is cancer stem cell markers related to intracellular signaling pathways and cancer metastasis mechanisms. Also, we are searching for new cancer stem cell markers and cancer stem cell marker-mediated therapeutic targets.

Various in vitro studies based on molecular biology are performed by qualified members in the affluent facility of our institution. Furthermore, cancer tissue and blood samples, clinicopathological and radiological findings, and survival information can be analyzed and compared to in vitro / in vivo animal data. These precious clinical data could be used to verify and strengthen our in vitro and in vivo animal work.

  1. Research on the relationship between hepatic cancer stemness and tumor microenvironment
2. Research on the telomere length change and the role of telomere-related protein in
3. Research on the activation mechanism of hepatic cancer stemness from epithelial-mesenchymal
  transition and tumor microenvironment
4. Research on tumor suppressor gene expression and its control mechanism in hepatic cancer stem
  cells related to tumor microenvironment and inflammatory cytokines.

Cancer stem cells have the ability to self-renew, differentiate, and proliferate and have a great potential for tumorigenesis in many cancers. Because cancer stem cells are resistant to chemotherapy and radiotherapy, such properties of cancer stem cells are considered as possible causes of metastasis and recurrence of cancers. Increasing evidence shows that eliminating cancer stem cells is the key to cure cancer. (Figure 1)


Environment-mediated drug resistance (EMDR) due to cancer cell stemness and tumor microenvironment consists of two categories: one is soluble factor-mediated drug resistance (SFM-DR) mediated by cytokines, chemokines, and growth factors, and another is cancer adhesion-mediated drug resistance (CAM-DR) (Figure 2).


Cancer cells can acquire resistance in an early stage of therapy through not only the genetic alteration of cancer but also EMDR; finally, acquired resistance is developed in minimal residual disease after the treatment. If we were able to understand the interaction of cytokines, chemokines, abnormal signaling through stroma, and cancer stemness, we might overcome chemoresistance of cancer cell.


Chromosomes have specific construct called telomere. It is shortened as cells repeat mitosis and causes senescence and apoptosis in case of normal cells. In contrast, telomere is not shortened after mitosis in cancer cells. Telomerase, a well-known enzyme, takes an important role in this phenomenon. Telomere length is regulated by hexamer protein complex called shelterin complex. Human PinX1 is a promising target for cancer therapy because it is a TRF1-interacting protein, one of the shelterin complex, and suppresses telomerase.


We are investigating the role of PinX1 in telomere length regulation and preservation. Overexpression of PinX1 in cancer cells increases TRF1-telomere binding and is possibly related with the stability of TRF1 protein. We are studying TRF1 stability and telomere structure and length following PinX1 over- or down-expression.