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Phosphatase and tensin homolog overexpression decreases proliferation and invasion and increases apoptosis in oral squamous cell carcinoma cells.

Gao Q, Zhang L, Zhang B, Wang QY, Sun CF, Dong XT, Ying J - Oncol Lett (2014)

Bottom Line: PTEN expression was found to induce apoptosis in SCC-4 cells, possibly via negative regulation of the phosphatidylinositide 3-kinase/Akt signaling pathway and increased expression of Bcl-2-interacting mediator of cell death.In addition, PTEN was found to control the epithelial-mesenchymal transition in SCC cells, thereby reducing their invasive ability.Furthermore, Transwell assay revealed that the expression of E-cadherin was increased, while the expression of vimentin and SNAIL was decreased.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry, Liaoning Medical University, Jinzhou, Liaoning 121001, P.R. China.

ABSTRACT
Phosphatase and tensin homolog (PTEN) is a potent tumor suppressor which regulates various cellular functions. The aim of the present study was to analyze the function of PTEN gene expression in squamous cell carcinoma (SCC) cells. This gene exhibits a unique function in cell migration and proliferation during the early stages of embryonic development. However, its role as a tumor suppressor gene in tongue squamous carcinoma cells remains unclear. In the present study, an SCC-4 cell line stably expressing PTEN was established and the effects of PTEN gene expression on SCC-4 cell proliferation, invasion and apoptosis were investigated. PTEN expression was found to induce apoptosis in SCC-4 cells, possibly via negative regulation of the phosphatidylinositide 3-kinase/Akt signaling pathway and increased expression of Bcl-2-interacting mediator of cell death. In addition, PTEN was found to control the epithelial-mesenchymal transition in SCC cells, thereby reducing their invasive ability. Furthermore, Transwell assay revealed that the expression of E-cadherin was increased, while the expression of vimentin and SNAIL was decreased. This study has provided an important insight into the mechanisms by which PTEN mediates the progression and early metastasis of tongue carcinoma.

No MeSH data available.


Related in: MedlinePlus

(A) Effects of PTEN expression on E-cadherin, SNAIL and vimentin proteins levels in SCC-4 cells. Untransfected cells (lane 1) and cells transfected with empty vector (lane 2) or PTEN (lane 3) were subjected to western blotting using the indicated antibodies. β-Actin was used as a loading control. (B) Quantification of E-cadherin, SNAIL and vimentin protein expression. PTEN, phosphatase and tensin homolog; SCC, squamous cell carcinoma; pEGFP, phosphorylated enhanced green fluorescent protein; OD, optical density.
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f6-ol-08-03-1058: (A) Effects of PTEN expression on E-cadherin, SNAIL and vimentin proteins levels in SCC-4 cells. Untransfected cells (lane 1) and cells transfected with empty vector (lane 2) or PTEN (lane 3) were subjected to western blotting using the indicated antibodies. β-Actin was used as a loading control. (B) Quantification of E-cadherin, SNAIL and vimentin protein expression. PTEN, phosphatase and tensin homolog; SCC, squamous cell carcinoma; pEGFP, phosphorylated enhanced green fluorescent protein; OD, optical density.

Mentions: Cells in the control group (SCC-4), empty vector group (pEGFP-SCC-4) and transfected group (pEGFP-PTEN-SCC-4) were cultured in Transwell invasion chambers for 36 h. For the 30 visually selected fields from each group, the numbers of cells invading through the membrane were 82±5, 80±4 and 42±5, respectively (Fig. 2C). These results demonstrated that PTEN expression caused a significant reduction in SCC-4 invasion when compared with the control (P<0.01). In addition, a statistically significant difference was identified when comparing the expression of the three proteins in the transfected and control groups (P<0.05). However, no significant differences were identified between the protein expression of the empty vector and control groups (P>0.05). The results of the western blotting revealed that PTEN expression significantly induced the expression of E-cadherin (SCC-4, 0.556±0.022; pEGFP-SCC-4, 0.573±0.013; and pEGFP-PTEN-SCC-4, 1.375±0.026) and suppressed the expression of SNAIL (SCC-4, 1.554±0.041; pEGFP-SCC-4, 1.412±0.036; and pEGFP-PTEN-SCC-4, 0.801±0.027) and vimentin (SCC-4, 1.667±0.045; pEGFP-SCC-4, 1.593±0.013; and pEGFP-PTEN-SCC-4, 0.778±0.032) (P<0.01) (Fig. 6). These results suggested that PTEN may block OTSCC cell invasion by inhibiting the EMT process.


Phosphatase and tensin homolog overexpression decreases proliferation and invasion and increases apoptosis in oral squamous cell carcinoma cells.

Gao Q, Zhang L, Zhang B, Wang QY, Sun CF, Dong XT, Ying J - Oncol Lett (2014)

(A) Effects of PTEN expression on E-cadherin, SNAIL and vimentin proteins levels in SCC-4 cells. Untransfected cells (lane 1) and cells transfected with empty vector (lane 2) or PTEN (lane 3) were subjected to western blotting using the indicated antibodies. β-Actin was used as a loading control. (B) Quantification of E-cadherin, SNAIL and vimentin protein expression. PTEN, phosphatase and tensin homolog; SCC, squamous cell carcinoma; pEGFP, phosphorylated enhanced green fluorescent protein; OD, optical density.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4114615&req=5

f6-ol-08-03-1058: (A) Effects of PTEN expression on E-cadherin, SNAIL and vimentin proteins levels in SCC-4 cells. Untransfected cells (lane 1) and cells transfected with empty vector (lane 2) or PTEN (lane 3) were subjected to western blotting using the indicated antibodies. β-Actin was used as a loading control. (B) Quantification of E-cadherin, SNAIL and vimentin protein expression. PTEN, phosphatase and tensin homolog; SCC, squamous cell carcinoma; pEGFP, phosphorylated enhanced green fluorescent protein; OD, optical density.
Mentions: Cells in the control group (SCC-4), empty vector group (pEGFP-SCC-4) and transfected group (pEGFP-PTEN-SCC-4) were cultured in Transwell invasion chambers for 36 h. For the 30 visually selected fields from each group, the numbers of cells invading through the membrane were 82±5, 80±4 and 42±5, respectively (Fig. 2C). These results demonstrated that PTEN expression caused a significant reduction in SCC-4 invasion when compared with the control (P<0.01). In addition, a statistically significant difference was identified when comparing the expression of the three proteins in the transfected and control groups (P<0.05). However, no significant differences were identified between the protein expression of the empty vector and control groups (P>0.05). The results of the western blotting revealed that PTEN expression significantly induced the expression of E-cadherin (SCC-4, 0.556±0.022; pEGFP-SCC-4, 0.573±0.013; and pEGFP-PTEN-SCC-4, 1.375±0.026) and suppressed the expression of SNAIL (SCC-4, 1.554±0.041; pEGFP-SCC-4, 1.412±0.036; and pEGFP-PTEN-SCC-4, 0.801±0.027) and vimentin (SCC-4, 1.667±0.045; pEGFP-SCC-4, 1.593±0.013; and pEGFP-PTEN-SCC-4, 0.778±0.032) (P<0.01) (Fig. 6). These results suggested that PTEN may block OTSCC cell invasion by inhibiting the EMT process.

Bottom Line: PTEN expression was found to induce apoptosis in SCC-4 cells, possibly via negative regulation of the phosphatidylinositide 3-kinase/Akt signaling pathway and increased expression of Bcl-2-interacting mediator of cell death.In addition, PTEN was found to control the epithelial-mesenchymal transition in SCC cells, thereby reducing their invasive ability.Furthermore, Transwell assay revealed that the expression of E-cadherin was increased, while the expression of vimentin and SNAIL was decreased.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry, Liaoning Medical University, Jinzhou, Liaoning 121001, P.R. China.

ABSTRACT
Phosphatase and tensin homolog (PTEN) is a potent tumor suppressor which regulates various cellular functions. The aim of the present study was to analyze the function of PTEN gene expression in squamous cell carcinoma (SCC) cells. This gene exhibits a unique function in cell migration and proliferation during the early stages of embryonic development. However, its role as a tumor suppressor gene in tongue squamous carcinoma cells remains unclear. In the present study, an SCC-4 cell line stably expressing PTEN was established and the effects of PTEN gene expression on SCC-4 cell proliferation, invasion and apoptosis were investigated. PTEN expression was found to induce apoptosis in SCC-4 cells, possibly via negative regulation of the phosphatidylinositide 3-kinase/Akt signaling pathway and increased expression of Bcl-2-interacting mediator of cell death. In addition, PTEN was found to control the epithelial-mesenchymal transition in SCC cells, thereby reducing their invasive ability. Furthermore, Transwell assay revealed that the expression of E-cadherin was increased, while the expression of vimentin and SNAIL was decreased. This study has provided an important insight into the mechanisms by which PTEN mediates the progression and early metastasis of tongue carcinoma.

No MeSH data available.


Related in: MedlinePlus