Jun He
Thomas Jefferson University, PA·Biochemistry
Triple-negative breast cancer lacks the three receptors that most breast cancer drugs target, so patients are treated mainly with chemotherapy and radiation, and tumors that resist those treatments leave few options. This cancer accounts for 15–20% of breast cancers and has lower survival.
- Fields
Biochemistry
Genetics
Medicine & Clinical Research
- Topics
triple negative breast cancer
miR-152
microRNA
- Grants
- 1 known grant, through Mar 2027
What they work on
- Determine how suppression of the microRNA miR-152 confers resistance to doxorubicin chemotherapy and radiation in triple-negative breast cancer cells, and test whether EZH2 and DNA hypermethylation are responsible for silencing miR-152.
- Test whether loss of miR-152 drives alternative splicing toward the PKM2 form of pyruvate kinase, switching cells to the Warburg effect (inefficient sugar burning) and supporting tumor growth and treatment resistance.
- Define how the miR-152/SLC7A5/PTBP1 pathway, involving an amino-acid transporter and an RNA-binding splicing regulator, controls metabolic reprogramming and response to doxorubicin and radiation.
- Test whether miR-152 loss and PKM2 induction promote tumor blood-vessel growth via the signaling protein CXCL8, using a humanized chimeric tumor model.
- Measure whether levels of miR-152, PKM2, HIF-1α, hnRNPA3, SLC7A5 and PTBP1 correlate with one another and with therapeutic response, cancer stage and survival in patient tumor tissue and patient-derived xenografts.
More about the research
A central question here is why these tumors resist treatment, and the proposed answer involves a small regulatory RNA molecule that normally keeps several growth- and metabolism-promoting proteins in check.
Why it matters
Patients with triple-negative breast cancer often stop responding to doxorubicin chemotherapy and radiation, and have poorer survival than other breast cancer patients. By mapping how loss of the microRNA miR-152 raises PKM2, SLC7A5 and PTBP1 to rewire tumor metabolism and blunt treatment, the work could identify molecules to target alongside existing therapy, and markers that correlate with treatment response, cancer stage and survival.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Yaguang Xi
University of Georgia, GA·Pharmacology
Determine how the oncogenic microRNA miR-10b and its target gene NR4A3 contribute to the experimental compound LG007's activity against triple-negative breast cancer.
Ramesh Ganju
Ohio State University, OH·Microbiology & Immunology
Determine how S100A7 signaling controls genes that respond to interferon-gamma, especially PD-L1 and Fas, in African American TNBC cells and in engineered mice that overproduce mouse S100a7.
Sanchita Bhatnagar
University of California-Davis, CA·Medicine & Clinical Research
Screen TRIM37 gene variants already identified in African American women for anoikis resistance, the ability of cancer cells to survive after detaching, and compare how risk and reference alleles of TRIM37 behave biologically.
The school
Thomas Jefferson University: 12 labs on PI Pages, $271M a year on research, 33 research doctorates a year.
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