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Triple-negative breast cancers (TNBCs) are tumors that lack the estrogen-receptor (ER), the progesterone-receptor (PR), and the epithelial growth factor receptor 2 (HER2) and are responsible for 15-20% of all breast cancer. TNBCs provide poor prognoses and higher rates for metastases compared to other breast cancers. We have found that cytoplasmic polyadenylation element binding protein 2 (CPEB2) mRNA splicing is dysregulated in cells that display resistance to anoikis (attachment-dependent cell death). Importantly, CPEB2A:B ratio decreases in patient-matched tumor tissue when compared to normal control tissue. Furthermore, downregulation of each isoform produced opposing effects on both AnR and HIF1alpha and TWIST1 levels (molecules that are downstream of CPEB2). Taken together, our results indicate that CPEB2 is involved in the development of anoikis-resistance in cancer cells and may be heavily involved in TNBC cancer progression. Additional studies of alternative splicing in TNBC may lead to both understanding of the molecular pathways leading to TNBC metastasis and the development of rationally designed treatments for TNBC.

Publication Date


Subject Major(s)

Cancer/Cellular Biology

Current Academic Year


Faculty Advisor/Mentor

Margaret Park

Faculty Advisor/Mentor

Sarah Golding


Virginia Commonwealth University. Undergraduate Research Opportunities Program

Is Part Of

VCU Undergraduate Research Posters


© The Author(s)

Cytoplasmic Polyadenylation Element Binding (CPEB) Protein 2 splice variants CPEB2A and CPEB2B affect the hypoxic response and triple-negative breast cancer metastasis