Epithelial-mesenchymal transition in cervical carcinoma.

During the progression of epithelial cancer, cells usually lose epithelial characteristic features and gain a mesenchymal phenotype. Cervical cancer is a common female malignancy worldwide. Despite the generally good prognosis for early-stage cervical cancer patients, many patients still die as a result of metastasis and recurrence. Epithelial-mesenchymal transition (EMT) has been implicated in the metastasis of primary tumors and provides molecular mechanisms for cervical cancer metastasis. Here we provide an up-to-date overview regarding the program of EMT in cervical cancer. In the stepwise progression of cervical cancer, human papilloma viral proteins contribute to the cell transformation and the conversion of typical epithelial cells to the epithelial carcinoma cells with hybrid epithelial and mesenchymal characteristics. Molecules related to the EMT program of cervical cancer cells are summarized in this review paper. Several soluble factors acting on their cognate receptors stimulate the mesenchymal transition of cervical epithelial cells. Ion transport system as well as cytoskeletal modulators also stimulate the progression of EMT program in cervical carcinoma cells. Transcriptional factors such as Snail, Twist1, Twist2, and six1 homeoproteins are involved in the complicated regulation and cervical cancer metastasis. Among the various signalings associated with EMT program, Snail is a central transcription factor which governs EMT program. In contrast to tumor promoters, several tumor suppressors such as SFRP1/2 and LMX-1A have been reported to suppress tumorigenesis as well as metastatic spread through inhibiting the EMT program.