Inflammatory and Metabolic Pathways in Cancer

Principal Investigator: 
Jorge Moscat, Ph.D.

The signaling pathways that regulate inflammation and cell proliferation, and their interface with autophagy and metabolism, are central to the control of tumor initiation and progression as well as in the development of metastasis. The Moscat laboratory studies these processes in the context of the crosstalk between the tumor epithelium, the tumor stroma, and its immunological microenvironment. Emphasis is placed on colorectal and liver cancer. The lab pays particular attention to the role and mechanism of action of several key signaling molecules, which include the autophagy and signaling adapters p62 and NBR1, and their binding partners, the atypical protein kinase C isoforms PKCζ and PKCλ⁄ι. The study of these fundamental biological questions results in the identification of non-oncogenic vulnerabilities that will lead to the design of more efficacious and less toxic anti-cancer therapies by targeting not only the epithelium but also the tumor stroma.

Weill Cornell Medicine published Newsroom article on our research. Read it here!

Active Projects

  • Autophagy and cell survival in intestinal tumorigenesis
  • Stem cell populations and signaling in intestinal inflammation and cancer
  • Stromal activation and immune response in therapy resistance in colorectal cancer
  • Stromal control of the immunological microenvironment in liver cancer
  • Metabolic reprograming and oxidative stress in hepatocellular carcinoma
  • Identification and design of new anti-cancer drugs targeting the serine metabolism

Grants

PI: Jorge Moscat, PhD
The goal of this proposal is to investigate the role and mechanisms of action of p62 and NBR1 in the activation of hepatic stellate cells, and their impact during NASH and liver cancer development. 
R01DK108743 NIH/NIDDK 

PI: Jorge Moscat, PhD
This project will address the mechanisms through which p62 drives HCC development, focusing on the roles of NRF2 and mTORC1 as p62 effectors. Small molecules that interfere with p62-driven NRF2 and mTORC1 activation will be developed and evaluated their ability to prevent obesity-induced HCC in appropriate mouse models.
R01CA211794 NIH/NCI 

PI: Jorge Moscat, PhD
The scope of this study is to investigate the role and mechanism of action of PKCλ⁄ι as an essential regulator of autophagy and cell death in intestinal cell homeostasis and inflammation-driven tumorigenesis.
R01CA207177 NIH/NCI 

PI: Jorge Moscat, PhD
The scope of the proposed project is to identify inhibitors of PHGDH, a cancer metabolism target.
16X113-PHGDH NCI-NeXT Program 

PI: Jorge Moscat, PhD
The scope is to test the effect of PVHA in serrated tumors.
RCA 19-02 Haloyme, Inc. 

PI: Jorge Moscat, PhD
National Institutes of Health (R01)

Co-PI: Jorge Moscat, PhD
WCM Prostate Cancer SPORE Developmental Research Program



Lab Team

Inflammatory and Metabolic Pathways in Cancer Lab Team

Additional Key Academic Personnel

Shanka Chatterjee
Post Doc
ssc4002@med.cornell.edu
Tania Cid-Diaz
Post Doc
tcd4002@med.cornell.edu
M. Imran Khan
Post Doc
mok4006@med.cornell.edu
Hiroto Kinoshita
Post Doc
hik4002@med.cornell.edu
Anxo Martinez-Ordonez
Post Doc
amo4002@med.cornell.edu
Yu Muta
Post Doc
yum4002@med.cornell.edu
Sadaaki Nishimura
Post Doc
san4005@med.cornell.edu
Marta Osrodek
Post Doc
mao4009@med.cornell.edu
Marc Ruiz-Martinez
Post Doc
mar4020@med.cornell.edu
Xiao Zhang
Post Doc
xiz4007@med.cornell.edu

Photo Gallery

Contact Information

Jorge Moscat, Ph.D.
Vice Chair for Experimental Pathology
Homer T. Hirst III Professor of Oncology in Pathology
Rockefeller University

1230 York Avenue
Weiss 11th Floor
New York, NY 10065

Pathology & Laboratory Medicine 1300 York Avenue New York, NY 10065 Phone: (212) 746-6464
Surgical Pathology: (212) 746-2700