Yekaterina Zaytseva
University of Kentucky, KY·Medicine & Clinical Research
Most deaths from colorectal cancer (CRC) happen because the cancer spreads, most often to the liver, and current treatments rarely stop it from coming back there. This work asks how a tumor's fat-making machinery helps it spread.
- Fields
Medicine & Clinical Research
Biochemistry
Pharmacology
- Topics
colorectal cancer
metastasis
fatty acid synthase
- Grants
- 2 known grants, through May 2028
What they work on
- Determine whether FASN overproduction in colorectal cancer cells, through the exosomes they release, turns liver hepatic stellate cells into tumor-supporting fibroblasts, using genetic changes and the FASN inhibitor TVB-2640.
- Test whether FASN promotes colorectal cancer spread to the liver through cancer-cell exosomes in orthotopic and syngeneic mouse models of liver metastasis.
- Test whether FASN enhances colorectal cancer metastasis by boosting the SphK/S1P pathway, which makes the signaling fat sphingosine-1-phosphate, and define the separate roles of SphK1 and SphK2.
- Determine how FASN controls CD36, a protein that imports outside fats, and how rising CD36 drives metastasis and S1P production, using metabolomics and isotope tracing.
- Test whether blocking fat uptake through CD36 makes the FASN inhibitor TVB-3664 more effective against colorectal cancer, using patient-derived cells, tumor organoids and metastasis models.
More about the research
It centers on fatty acid synthase (FASN), the enzyme that builds palmitate, a basic fat that cells use to make membranes and to store energy. FASN is overproduced in colorectal tumors and linked to metastasis and poor survival. The lab has shown that higher FASN levels are a key mechanism supporting colorectal cancer metastasis. Its two projects follow how FASN affects signaling fats, fat uptake, and the tiny packages that tumors send to distant organs.
Why it matters
Colorectal cancer is the second most common cause of cancer death in the United States, mostly because of metastasis. FASN inhibitors such as TVB-2640 and CD36 inhibitors are already in clinical trials. Knowing how FASN drives spread to the liver, and how tumors may resist these drugs, could guide better drug combinations and new targets for patients with metastatic colorectal cancer and possibly other solid tumors.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Rui Wang
Case Western Reserve University, OH·Pharmacology
Determine whether LRG1 secreted by liver endothelial cells drives colorectal cancer liver metastases to start and grow, using mice lacking endothelial LRG1 and an LRG1-neutralizing antibody.
Pankaj Singh
University of Oklahoma-Health Sciences Center, OK·Biochemistry
Test whether blocking PADI1, an enzyme that chemically modifies arginine in proteins, or its downstream metabolic pathways prevents FOLFIRINOX resistance in pancreatic cancer cells, organoids and patient-derived xenografts.
Christopher LaRocca
University of Minnesota, MN·Medicine & Clinical Research·Early-career
Identify which viral fiber structure, the part that attaches the virus to a cell, and which promoter, the genetic switch driving replication, give the strongest and most selective infection of human colorectal cancer cells, using cancer cell lines and patient-derived tissue slices.
The school
University of Kentucky: 34 labs on PI Pages, $528M a year on research, 319 research doctorates a year.
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