Lucia R. Languino
Thomas Jefferson University, PA·Biology
Some prostate cancers stop depending on male hormones after hormone-blocking treatment. They turn into neuroendocrine prostate cancer (NEPC), an aggressive form that spreads quickly to bone and other organs and resists therapy.
- Fields
Biology
Medicine & Clinical Research
Pharmacology
- Topics
prostate cancer
metastasis
extracellular vesicles
- Grants
- 2 known grants, through Feb 2031
What they work on
- Test whether NgR2 carried in small extracellular vesicles causes tumor growth, neuroendocrine differentiation, and metastasis after transfer to other cells, using SILAC-based proteomics.
- Measure the active state of αVβ3 integrin in vesicles, including those in human plasma, using ExoView chips that analyze single vesicles by their interaction with NgR2.
- Determine whether vesicle-delivered αVβ3 and NgR2 switch on RhoA and JAK/STAT signaling in recipient cells, and whether these pathways are needed for the shift to a neuroendocrine state.
- Examine how αVβ3 and NgR2 relate to IL-4 production in progressing human tumors, and how they affect T cells, monocytes, tumor growth, and immunity in mouse prostate cancer models.
More about the research
At least a quarter of patients whose disease progresses after hormone suppression develop it, and life expectancy is often seven months or less. There are no effective treatments. This research asks how prostate cancer cells 'talk' to surrounding cells, and how that conversation drives the shift to NEPC and its spread.
Why it matters
Patients with metastatic neuroendocrine prostate cancer have no effective treatment options and very short survival, and the condition may grow more common as stronger hormone-blocking drugs come into use. Identifying the αVβ3 integrin–NgR2 vesicle pathway and other vulnerabilities could validate new drug targets. Vesicle markers found in blood could also help track the disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Feng Yang
Baylor College of Medicine, TX·Medicine & Clinical Research
Determine how COP1, an E3 ubiquitin ligase, binds and tags GATA2 for degradation in prostate cancer cells, including castration-resistant and taxane-resistant models.
Susan Logan
New York University, NY·Pharmacology
Test whether macrocycle 13, a synthetic ring-shaped molecule designed to block beta-catenin from binding its DNA partner TCF, suppresses Wnt/beta-catenin signaling in in vivo models of castration-resistant prostate cancer.
Scott Dehm
University of Minnesota, MN·Medicine & Clinical Research
Determine how AR-blocking therapies induce KLF5, a stem cell transcription factor, and lineage plasticity traits in castration-resistant prostate cancer cells.
The school
Thomas Jefferson University: 12 labs on PI Pages, $271M a year on research, 33 research doctorates a year.
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