Matossian M, Hoang VT, Burks HE, La J, Elliott S, Brock C, Rusch DB, Buechlein A, Nephew KP, Bhatt A, Cavanaugh JE, Flaherty PT, Collins-Burow BM, & Burow ME. Constitutive activation of MEK5 promotes a mesenchymal and migratory cell phenotype in triple negative breast cancer. Oncoscience (2021)

How they used Xena

They used Xena to make Figure 1, where they explored the relationship between MEK5, the TFAC30 gene expression signature, and patient survival.

Part of Figure 1 from the paper

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Paper

Constitutive activation of MEK5 promotes a mesenchymal and migratory cell phenotype in triple negative breast cancer.

Triple negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited targeted therapeutic options. A defining feature of TNBC is the propensity to metastasize and acquire resistance to cytotoxic agents. Mitogen activated protein kinase (MAPK) and extracellular regulated kinase (ERK) signaling pathways have integral roles in cancer development and progression. While MEK5/ERK5 signaling drives mesenchymal and migratory cell phenotypes in breast cancer, the specific mechanisms underlying these actions remain under-characterized. To elucidate the mechanisms through which MEK5 regulates the mesenchymal and migratory phenotype, we generated stably transfected constitutively active MEK5 (MEK5-ca) TNBC cells. Downstream signaling pathways and candidate targets of MEK5-ca cells were based on RNA sequencing and confirmed using qPCR and Western blot analyses. MEK5 activation drove a mesenchymal cell phenotype independent of cell proliferation effects. Transwell migration assays demonstrated MEK5 activation significantly increased breast cancer cell migration. In this study, we provide supporting evidence that MEK5 functions through FRA-1 to regulate the mesenchymal and migratory phenotype in TNBC.