In healthy cells, TGF-beta signaling is crucial to the cell cycle. The pathway promotes apoptosis, suppresses cellular proliferation, and stimulates immune cell activation. In malignant cells, however, TGF-beta signaling has been shown to drive the proliferation of cancer through migration and metastasis, immune evasion, and angiogenesis. The effects of TGF-beta signaling shift from tumor-suppressing to tumor-promoting as cancer progresses. Using TCGA data, we identified genes coexpressed with TbetaRIII. After determining which genes had the highest correlation, we used Enrichr to conduct pathway analysis. Pathway analysis indicated a relationship with ERG, leading us to hypothesize that ERG regulates TbetaRIII and other related genes. ERG seems to share many cancer behaviors with TGF-beta, such as proliferation, invasion, and overall cell survival in cervical cancer. Kaplan-Meier Survival plots of TCGA data support decreased survival rates with high ERG expression in several other cancers as well, for the scope of this study, cervical cancer specifically. However, ERG has not been extensively investigated in this context. Western Blot analysis confirmed the presence of ERG expression in HeLa cells. Functional assays demonstrated that manipulating HeLa cells to express a knockdown of ERG led to a significant decrease in cell migration. The addition of TGF-beta to HeLa cells with ERG knockdown (shERG) partially restores migration, suggesting that TGF-beta could potentially compensate for the loss of ERG expression. To further investigate the effects of ERG on TGF-beta, galunisertib, a known inhibitor of TGF-beta signaling, was used. Analysis of scratch assays showed that in control HeLa cells, migration rates significantly reduced when exposed to galunisertib. In HeLa-shERG cells, migration was reduced as well; however, galunisertib failed to have the same decreased migration pattern in HeLa-shERG cells, suggesting that ERG and TGF-beta pathways may converge in some way. HeLa-shERG significantly reduced the expression of TGFbeta-I as well as decreasing the activation of SMAD2, a transcription factor that plays a significant role in TGF-beta signaling. Invasion assays exposed HeLa cells' ability to travel throughout the extracellular matrix when manipulating TGF-beta and ERG to measure metastasis. ChIP-seq is being done to investigate the possible interactions between TGFB signaling and ERG occupancy on the genome in cervical cancer, which will be compared to ERG sites in extensively studied cancers. Together, these findings suggest that ERG promotes cervical cancer cell migration and invasion, at least in part by regulating TGF-beta signaling.