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SOX2 enhances the migration and invasion of ovarian cancer cells via Src kinase.

Wang X, Ji X, Chen J, Yan D, Zhang Z, Wang Q, Xi X, Feng Y - PLoS ONE (2014)

Bottom Line: The results showed that the expression of SOX2 in primary tumors is much lower than that in the corresponding metastatic lesions.We further found that SOX2 overexpression promotes proliferation, migration and invasion, while inhibiting adhesion abilities of SOC cells.Together, these results suggested that Src kinase is a key molecule in SOX2-mediated migration and invasion of SOC cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Obstetrics and Gynecology, Shanghai Jiao Tong University Affiliated First People's Hospital, Shanghai, China.

ABSTRACT
Ovarian cancer is the leading cause of death among gynecologic cancers and is the fifth leading cause of all cancer-related deaths among women. The development of novel molecular targets is therefore important to many patients. Recently, the SRY-related transcription factor SOX2 has been widely reported to be involved in multiple pathophysiological diseases, including maintenance of stem cell characteristics and carcinogenesis. Up to now, SOX2 has been mainly shown to promote the development of cancer, although its inhibitory roles in cancer have also been reported. However, the role of SOX2 in ovarian cancer is largely unknown. In the present study, we detected the expression of SOX2 in 64 human serous ovarian carcinoma (SOC) tissues and paired corresponding metastatic specimens using immunohistochemistry. The results showed that the expression of SOX2 in primary tumors is much lower than that in the corresponding metastatic lesions. We further found that SOX2 overexpression promotes proliferation, migration and invasion, while inhibiting adhesion abilities of SOC cells. Finally, we found that SOX2 targets Src kinase, a non-receptor tyrosine kinase that regulates cell migration, invasion and adhesion in SOC cells. Together, these results suggested that Src kinase is a key molecule in SOX2-mediated migration and invasion of SOC cells.

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SOX2 decrease adhesion in SOC cells.(A) Decrease adhesion after stable transfection of SOX2 plasmid in HO8910. (B) Increase adhesion after transient transfection of SOX2 siRNA in HO8910-pm. (C) Increase adhesion after transient transfection of SOX2 siRNA in Skov3.
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pone-0099594-g005: SOX2 decrease adhesion in SOC cells.(A) Decrease adhesion after stable transfection of SOX2 plasmid in HO8910. (B) Increase adhesion after transient transfection of SOX2 siRNA in HO8910-pm. (C) Increase adhesion after transient transfection of SOX2 siRNA in Skov3.

Mentions: To further investigate the function of SOX2 in SOC cells, the SOX2 gene was overexpressed by lentiviral infection in Ho8910, which was confirmed by real-time PCR and Western blotting (Figure 2C). Subsequently, we determined the effect of SOX2 overexpression on the proliferation of the SOC cells. The results showed that overexpression of the SOX2 gene could promote SOC cell proliferation (Figure 3A and Figure 3B). Furthermore, we examined the effect of SOX2 overexpression on the migratory, invasive and adhesive abilities of the SOC cells using transwell assays and cell-ECM adhesion assays. The results showed that overexpression of SOX2 protein could significantly promote the migration and invasion of SOC cells (Figure 4A), while decreasing the adhesion of SOC cells to Matrigel, fibronectin, type I collagen and laminin(Figure 5A).


SOX2 enhances the migration and invasion of ovarian cancer cells via Src kinase.

Wang X, Ji X, Chen J, Yan D, Zhang Z, Wang Q, Xi X, Feng Y - PLoS ONE (2014)

SOX2 decrease adhesion in SOC cells.(A) Decrease adhesion after stable transfection of SOX2 plasmid in HO8910. (B) Increase adhesion after transient transfection of SOX2 siRNA in HO8910-pm. (C) Increase adhesion after transient transfection of SOX2 siRNA in Skov3.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4061006&req=5

pone-0099594-g005: SOX2 decrease adhesion in SOC cells.(A) Decrease adhesion after stable transfection of SOX2 plasmid in HO8910. (B) Increase adhesion after transient transfection of SOX2 siRNA in HO8910-pm. (C) Increase adhesion after transient transfection of SOX2 siRNA in Skov3.
Mentions: To further investigate the function of SOX2 in SOC cells, the SOX2 gene was overexpressed by lentiviral infection in Ho8910, which was confirmed by real-time PCR and Western blotting (Figure 2C). Subsequently, we determined the effect of SOX2 overexpression on the proliferation of the SOC cells. The results showed that overexpression of the SOX2 gene could promote SOC cell proliferation (Figure 3A and Figure 3B). Furthermore, we examined the effect of SOX2 overexpression on the migratory, invasive and adhesive abilities of the SOC cells using transwell assays and cell-ECM adhesion assays. The results showed that overexpression of SOX2 protein could significantly promote the migration and invasion of SOC cells (Figure 4A), while decreasing the adhesion of SOC cells to Matrigel, fibronectin, type I collagen and laminin(Figure 5A).

Bottom Line: The results showed that the expression of SOX2 in primary tumors is much lower than that in the corresponding metastatic lesions.We further found that SOX2 overexpression promotes proliferation, migration and invasion, while inhibiting adhesion abilities of SOC cells.Together, these results suggested that Src kinase is a key molecule in SOX2-mediated migration and invasion of SOC cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Obstetrics and Gynecology, Shanghai Jiao Tong University Affiliated First People's Hospital, Shanghai, China.

ABSTRACT
Ovarian cancer is the leading cause of death among gynecologic cancers and is the fifth leading cause of all cancer-related deaths among women. The development of novel molecular targets is therefore important to many patients. Recently, the SRY-related transcription factor SOX2 has been widely reported to be involved in multiple pathophysiological diseases, including maintenance of stem cell characteristics and carcinogenesis. Up to now, SOX2 has been mainly shown to promote the development of cancer, although its inhibitory roles in cancer have also been reported. However, the role of SOX2 in ovarian cancer is largely unknown. In the present study, we detected the expression of SOX2 in 64 human serous ovarian carcinoma (SOC) tissues and paired corresponding metastatic specimens using immunohistochemistry. The results showed that the expression of SOX2 in primary tumors is much lower than that in the corresponding metastatic lesions. We further found that SOX2 overexpression promotes proliferation, migration and invasion, while inhibiting adhesion abilities of SOC cells. Finally, we found that SOX2 targets Src kinase, a non-receptor tyrosine kinase that regulates cell migration, invasion and adhesion in SOC cells. Together, these results suggested that Src kinase is a key molecule in SOX2-mediated migration and invasion of SOC cells.

Show MeSH
Related in: MedlinePlus