Xin Chen, PhD

Xin Chen, PhD

This email address is being protected from spambots. You need JavaScript enabled to view it. | (808) 564-3804 | Chen Laboratory website

Program Co-Leader, Cancer Biology Program, University of Hawaiʻi Cancer Center
Full Member, Cancer Biology Program, University of Hawaiʻi Cancer Center

Academic Appointment(s):
Professor, (Researcher), Cancer Biology Program, University of Hawaiʻi Cancer Center

PhD, Harvard University
Postdoc Fellow, Howard Hughes Medical Institute, Stanford University

Research Focus

Our lab studies molecular genetics and signaling pathways during liver cancer growth to develop new therapies to treat this deadly disease.

Visit Chen Laboratory page

Based on genomic studies from human liver cancers using both in vitro cell culture system and in vivo modeling, we are characterizing the functional contribution of major signaling and metabolic cascades that contribute to hepatocarcinogenesis. We are studying pathways that include:

  1. PI3K/AKT/mTOR
  2. Hippo/Yap
  3. Notch
  4. Ras/MAPK
  5. β-catenin signaling.

We are studying the genetic and biochemical crosstalk among these pathways and how they regulate liver cancer development, and we are testing novel, targeted therapies for liver cancer treatment using drugs which specifically target these pathways.

Translational studies of human liver cancers:  bedside to the bench, and back to the bedside.
Translational studies of human liver cancers:  bedside to the bench, and back to the bedside.

Why now

Liver cancer is the fifth-most-common cancer and the third leading cause of cancer death worldwide. The molecular mechanisms underlying liver cancer development remains poorly understood. Treatment options for liver cancer are very limited and generally ineffective. Sorafenib is the only approved targeted therapeutic drug for liver cancer. However, it only prolongs the survival of patients with advanced liver cancer for about three months, and it is very expensive. It is of great importance to elucidate the mechanisms leading to hepatic carcinogenesis and identify novel therapeutic targets for the treatment of this malignancy.

Selected Publications

Zhang Y, Xu H, Liang B, Chen X, Ko S, Gui G, Wang P, Wang H, Xu M, Wnag J, Pes GM, Ribback S, Zeng Y, Singhi A, Monga SP, Evert M, Tang L, Calvisi DF, Chen X. (2022). β-Catenin sustains and is required for YAP oncogenic activity in cholangiocarcinoma. Gastroenterology; Epub 2022 Apr. Pubmed summary

Wang H, Zhou Y, Xu H, Wang X, Zhang Y, Shang R, O’Farrell M, Roessler S, Sticht C, Stahl A, Evert M, Calvisi DF, Zeng Y, Chen X. (2022). Therapeutic efficacy of FANS inhibition in preclinical models of HCC. Hepatol; Epub 2022 Jan. Pubmed summary

Wang H, Zhang S, Zhang Y, Jia J, Wang J, Liu X, Zhang J, Song X, Che L, Ribback S, Cigliano A, Evert M, Liang B, Wu H, Calvisi DF, Zeng Y, Chen X. (2022). TAZ is indispensable for hepatocarcinogenesis induced by c-MYC. J Hepatol; 76(1), Jan. 2022, 123-134. Pubmed summary

Song X, Wang P, Wang J, Affo S, Wang H, Xu M, Schwabe RF, Chang TT, Bogl M, Pes GM, Ribback S, Evert M, Chen X#, Calvisi DF# (#Co-corresponding authors). (2021). Focal adhesion kinase (FAK) promotes cholangiocarcinoma development and progression via YAP activation. J Hepatol; 75(4), pp888-899. Pubmed summary

Liang B, Zhou Y, Qian M, Xu M, Wang J, Zhang Y, Song X, Wang H, Lin S, Ren C, Monga SP, Wang B, Evert M, Chen Y, Chen X, Huang Z, Calvisi DF, Chen X. (2021). TBX3 functions as a tumor suppressor downstream of activated CTNNB1 mutants during hepatocarcinogenesis. J Hepatol; 75(1), pp120-131. Pubmed summary

Publication list via PubMed or MyNCIBibliography link

Active Grants

X. Chen, PI
“Investigating multifactorial beta-catenin activation in hepatocellular cancers”

X. Chen, PI
“Signaling pathways during hepatocarcinogenesis”

X.Chen, Co-PI (PI: Stahl, A)
“Role of protein mediated fatty acid uptake in liver cancer”

X. Chen, Co-PI (PI: Schwabe, R)
“Role of cancer-associated fibroblasts in cholangiocarcinoma”