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SOX-2 promotes epithelial-to-mesenchymal transition by modulating SLUG expression in esophageal squamous cells
Esophageal cancer is the sixth leading cause of cancer-related deaths worldwide, and majority of these cancers, arises from the squamous cells. Despite multiple therapeutic strategies, the five year survival rate of esophageal squamous cell carcinoma (ESCC) ranges between 15%-20%. Epithelial-mesenchymal transition (EMT) is one of the key events in ESCC, which is associated with recurrence, metastasis and low survival rate. Cancer stem cells (CSCs) are a heterogeneous population of cells within cancer that can differentiate into various types of cells and is often linked to metastasis and relapse. Earlier studies have reported that, cancer cells exhibiting EMT can acquire stem cell-like characteristic and express markers of EMT. However, the correlation between stemness and EMT is still unclear in ESCC. This study was done to evaluate if the cancer stem cell marker SOX-2 can promote EMT by modulating the expression of SLUG in Esophageal Squamous cells.
The ESCC cells (Eca-109) were used for transfection of SOX-2 coding DNA sequence, which was inserted into pCMV vector. The cell migration and invasion was evaluated using transwell migration chamber. The expression of EMT marker, SLUG, in cells overexpressing SOX-2, was measured using RT-PCR and Western blot. This was done to explore, if SLUG is involved in SOX-2 mediated regulation of EMT.
The Eca-109/pCMV-SOX2 cells showed higher levels of SOX2 mRNA, when compared to the Eca-109/pCMV, as demonstrated by RT-PCR. The transmigration assay revealed that Eca-109/pCMV – SOX2 cells, had increased invasive and migratory potential after 24 hours incubation. Our studies also showed that, higher expression of SLUG mRNA and protein, positively correlated with SOX-2 overexpression.
Our study demonstrates that, over expression of SOX-2 promotes invasion, migration and Epithelial-mesenchymal transition in ESCC cells, thus emphasizing the usefulness of SOX-2 as a potential therapeutic target in the treatment of ESCC.
The authors.
Has not received any funding.
All authors have declared no conflicts of interest.
