Pengda Liu

Pengda Liu, PhD, is a UNC Lineberger Comprehensive Cancer Center member and Assistant Professor in the Department of Biochemistry and Biophysics at UNC-Chapel Hill.

Pengda Liu

Assistant Professor
Department of Biochemistry and Biophysics
UNC-Chapel Hill
Cancer Cell Biology

21-237 Lineberger Building
450 West Drive
Chapel Hill, NC 27599

Area of interest

We are interested in deciphering the molecular mechanisms underlying aberrant signaling events that contribute to tumorigenesis mediated by protein modifications and protein-protein interactions. Understanding these events may lead to identification of novel drug targets and provide new treatment strategies to combat human cancer. To this end, we are interested in the potential of enzymes, and their inhibition, for generating traditional inhibitory chemical compounds or antibodies as potential therapeutic tools. Cell signaling networks determine cell fate and aberrant activation of oncogenic signaling is a key mechanism during cancer development; however, cell-signaling networks are complicated and dynamic with fluxes in both space and time. Thus, to understand how cancer-associated aberrant cell decisions are made requires addressing the following questions through a global view of cell signaling networks, including to identify the key molecular events that lead to malignant diseases but do not occur in healthy cells and to elucidate how can cancer-associated signaling modules be targeted for cancer treatment?

Research in biology has been revolutionized by interdisciplinary techniques and methods applied to biological questions. Previously we have employed multi-disciplinary approaches to illustrate a novel cell-cycle dependent activation mechanism for the oncoprotein kinase Akt, to reveal a critical role of Akt in governing genome stability by in part phosphorylating and destablizing XLF, a key component of the non-homologous end joining (NHEJ) repair complex, to demonstrate a direct role for PI(3,4,5)P3 to activate mTORC2, as well as to identify phosphorylation events to inactivate mTORC2. Together, these studies provide molecular bases for understanding how aberrant cell signaling events contribute to cancer development, as well as offer the rationale to develop novel anti-cancer therapies targeting specific cell signaling pathway components.

Moving forward, we are interested in developing new experimental systems and tools to further understand the interplays between key cancer signaling events to connect cancer signaling, metabolism and epigenetics, with the ultimate goal of identification and development of new targeted therapies to combat cancer.

Awards and Honors

  • 2017 Atomwise AIM Award
  • 2017 IBM Junior Faculty Development Award
  • 2016 East Carolina University 40 under 40 leadership award
  • 2014 NIH/NCI Howard Temin Pathway to Independence Award in Cancer Research Award
  • 2012 NIH/Ruth L. Kirschstein National Research Service Award (NRSA T32 Training Fellowship)
  • 2006 Carol F. Volkman Award

Find publications on PubMed