Abstract
Cervical cancer with early metastasis of the primary tumor is associated with poor prognosis and poor therapeutic outcomes. Since epithelial-to-mesenchymal transition (EMT) plays a role in acquisition of the ability to invade the pelvic lymph nodes and surrounding tissue, it is important to clarify the molecular mechanism underlying EMT in cervical cancer. RhoE, also known as Rnd3, is a member of the Rnd subfamily of Rho GTPases. While previous reports have suggested that RhoE may act as either a positive or a negative regulator of cancer metastasis and EMT, the role of RhoE during EMT in cervical cancer cells remains unclear. The present study revealed that RhoE expression was upregulated during transforming growth factor-β (TGF-β)-mediated EMT in human cervical cancer HeLa cells. Furthermore, reduced RhoE expression enhanced TGF-β-mediated EMT and migration of HeLa cells. In addition, we demonstrated that RhoE knockdown elevated RhoA activity and a ROCK inhibitor partially suppressed the acceleration of TGF-β-mediated EMT by RhoE knockdown. These results indicate that RhoE suppresses TGF-β-mediated EMT, partially via RhoA/ROCK signaling in cervical cancer HeLa cells.
Highlights
Cervical cancer is the third most common malignancy in women worldwide [1,2], and cervical cancer with early metastasis of the primary tumor is associated with poor prognosis and poor therapeutic outcomes [3,4]
Western blot and quantitative real-time polymerase chain reaction analyses showed higher expression levels of RhoE in cells treated with TGF-β1 for 72 h compared with the control cells, suggesting that RhoE expression is elevated during transforming growth factor-β (TGF-β)-induced Epithelial-to-mesenchymal transition (EMT) in HeLa cells (Figure 1)
Western blot and quantitative realtime polymerase chain reaction analyses showed higher expression levels of RhoE in cells treated with TGF-β1 for 72 h compared with the control cells, suggesting that RhoE expression is elevated during TGF-β-induced EMT in HeLa cells (Figure 1)
Summary
Cervical cancer is the third most common malignancy in women worldwide [1,2], and cervical cancer with early metastasis of the primary tumor is associated with poor prognosis and poor therapeutic outcomes [3,4]. Metastasis consists of sequential and selective steps, including local invasion, intravasation, circulation, extravasation, and colonization. Epithelial-to-mesenchymal transition (EMT) is an important step for intravasation of metastatic cancer cells into blood. During EMT, epithelial cells lose their polarity, cytoskeletal structure, and cell–cell adhesion and acquire migratory properties typical of mesenchymal cells [5,6,7]. It is thought that EMT plays a role in the acquisition of the ability to invade the pelvic lymph nodes and surrounding tissue in cervical cancer cells [1,2]. It is important to clarify the molecular mechanisms underlying EMT in cervical cancer
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