Jing Yang
University of California-San Diego, CA·Biochemistry
Breast cancer cells grow, spread and resist treatment by reading signals from inside and outside the cell. Most breast cancers depend on the estrogen receptor, a protein that drives growth in response to the hormone estrogen.
- Fields
Biochemistry
Medicine & Clinical Research
Biology
- Topics
breast cancer
estrogen receptor
hormone therapy resistance
- Grants
- 3 known grants, through Apr 2031
What they work on
- Determine how the Hippo pathway, through the LATS1/2 kinases, controls transcription of ESR1, the main estrogen receptor gene, in breast cells and what ESR1 contributes to Hippo biology in breast tissue.
- Test whether blocking LATS1/2 both slows ER+ breast cancer growth by lowering ESR1 and makes cancer cells more visible to the immune system, improving immunotherapy.
- Define how a stiff extracellular matrix activates the LYN kinase so that TWIST1, a protein that switches on cell-migration genes, enters the nucleus and drives epithelial-mesenchymal transition (EMT).
- Uncover how soft matrix keeps TWIST1 out of the nucleus and blocks EMT, revealing the other half of the stiffness-sensing switch in breast cancer cells.
- Test whether the TWIST1 mechanotransduction pathway drives metastasis in living animals and whether it predicts progression in human breast cancer.
More about the research
Drugs that block this receptor work at first, but tumors often become resistant. Tumors that spread to distant organs (metastasis) are also hard to treat. The projects here ask how two kinds of signals control breast cancer: a growth-control pathway that switches the estrogen receptor gene on, and the physical stiffness of the tissue around a tumor.
Why it matters
Patients with estrogen receptor–positive breast cancer often stop responding to hormone therapy, and metastasis drives most cancer deaths. This work could supply a basis for treating ER+ breast cancer with drugs that block the LATS1/2 kinases, possibly alongside immunotherapy. It could also reveal new targets in the stiffness-sensing LYN–TWIST1 pathway for drugs that slow tumor spread.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Sean Fanning
Loyola University Chicago, IL·Pharmacology
Determine how a library of more than 100 SERMs and SERDs bind to and reshape mutant Y537S estrogen receptor alpha, using X-ray co-crystal structures and anti-cancer assays in breast cancer cells.
Benjamin Spike
University of Utah, UT·Biology
Track how CRIPTO (CR1) drives cell state changes at different stages of breast cancer metastasis, using mouse transplant models with patient-derived cancer cells, bioengineered systems and single-cell RNA sequencing.
Deeann Wallis-Schultz
University of Alabama at Birmingham, AL·Genetics
Track tumor onset, growth, histology and molecular changes in Ras and estrogen signaling over time in Nf1 knockin (p.R1276Q) and knockout rats, comparing findings with human breast tumor samples.
The school
University of California-San Diego: 84 labs on PI Pages, $1.9B a year on research, 637 research doctorates a year.
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