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Vitamin E succinate induces apoptosis via the PI3K/AKT signaling pathways in EC109 esophageal cancer cells.

Yang P, Zhao J, Hou L, Yang L, Wu K, Zhang L - Mol Med Rep (2016)

Bottom Line: Furthermore, VES downregulated constitutively active basal levels of phosphorylated (p)‑serine‑threonine kinase AKT (AKT) and p‑mammalian target of rapamycin (mTOR), and decreased the phosphorylation of AKT substrates Bcl‑2‑associated death receptor and caspase‑9, in addition to mTOR effectors, ribosomal protein S6 kinase β1 and eIF4E‑binding protein 1.Phosphoinositide‑3‑kinase (PI3K) inhibitor, LY294002 suppressed p‑AKT and p‑mTOR, indicating PI3K is a common upstream mediator.Furthermore, the current study suggests that VES may be useful in a combinational therapeutic strategy employing an mTOR inhibitor.

View Article: PubMed Central - PubMed

Affiliation: Department of Thoracic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.

ABSTRACT
Esophageal cancer is the fourth most common gastrointestinal cancer, it generally has a poor prognosis and novel strategies are required for prevention and treatment. Vitamin E succinate (VES) is a potential chemical agent for cancer prevention and therapy as it exerts anti‑tumor effects in a variety of cancers. However, the role of VES in tumorigenesis and progression of cancer remains to be elucidated. The present study aimed to determine the effects of VES in regulating the survival and apoptosis of human esophageal cancer cells. EC109 human esophageal cancer cells were used to investigate the anti‑proliferative effects of VES. The MTT and Annexin V‑fluorescein isothiocyanate/propidium iodide assays demonstrated that VES inhibited cell proliferation and induced apoptosis in esophageal cancer cells. Furthermore, VES downregulated constitutively active basal levels of phosphorylated (p)‑serine‑threonine kinase AKT (AKT) and p‑mammalian target of rapamycin (mTOR), and decreased the phosphorylation of AKT substrates Bcl‑2‑associated death receptor and caspase‑9, in addition to mTOR effectors, ribosomal protein S6 kinase β1 and eIF4E‑binding protein 1. Phosphoinositide‑3‑kinase (PI3K) inhibitor, LY294002 suppressed p‑AKT and p‑mTOR, indicating PI3K is a common upstream mediator. The apoptosis induced by VES was increased by inhibition of AKT or mTOR with their respective inhibitor in esophageal cancer cells. The results of the present study suggested that VES targeted the PI3K/AKT signaling pathways and induced apoptosis in esophageal cancer cells. Furthermore, the current study suggests that VES may be useful in a combinational therapeutic strategy employing an mTOR inhibitor.

No MeSH data available.


Related in: MedlinePlus

VES inhibits the proliferation of EC-109 esophageal cancer cells. (A) Cells (1×104) were plated in 96-well plates containing 100 ml medium. Following incubation for 24 h, the cells were treated with varying concentrations of VES for 24 h and cell survival was evaluated using the MTT assay. (B) Cell viability was evaluated by MTT assay and presented as the mean ± standard deviation compared with untreated control cells. *P<0.05 vs. 0 µM VES group. VES, vitamin E succinate.
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f1-mmr-14-02-1531: VES inhibits the proliferation of EC-109 esophageal cancer cells. (A) Cells (1×104) were plated in 96-well plates containing 100 ml medium. Following incubation for 24 h, the cells were treated with varying concentrations of VES for 24 h and cell survival was evaluated using the MTT assay. (B) Cell viability was evaluated by MTT assay and presented as the mean ± standard deviation compared with untreated control cells. *P<0.05 vs. 0 µM VES group. VES, vitamin E succinate.

Mentions: The effects of VES on the EC109 human esophageal cancer cell line was detected in the present study. The IC50 value of VES was determined by treating EC109 cells with increasing concentrations of VES for 24 h. IC50 value was calculated to be 25.1 µM for EC109 cells at 24 h (Fig. 1A). EC109 cells were treated with 10–100 µM VES for 24 h, and the cell viability was evaluated by MTT assay. The results demonstrated that the growth was decreased by ~45 and ~81% following treatment with 10 and 100 µM VES in EC109 cells (Fig. 1B). The current study also investigated whether the proliferation inhibition resulted from the induction of apoptosis in the cells.


Vitamin E succinate induces apoptosis via the PI3K/AKT signaling pathways in EC109 esophageal cancer cells.

Yang P, Zhao J, Hou L, Yang L, Wu K, Zhang L - Mol Med Rep (2016)

VES inhibits the proliferation of EC-109 esophageal cancer cells. (A) Cells (1×104) were plated in 96-well plates containing 100 ml medium. Following incubation for 24 h, the cells were treated with varying concentrations of VES for 24 h and cell survival was evaluated using the MTT assay. (B) Cell viability was evaluated by MTT assay and presented as the mean ± standard deviation compared with untreated control cells. *P<0.05 vs. 0 µM VES group. VES, vitamin E succinate.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4940098&req=5

f1-mmr-14-02-1531: VES inhibits the proliferation of EC-109 esophageal cancer cells. (A) Cells (1×104) were plated in 96-well plates containing 100 ml medium. Following incubation for 24 h, the cells were treated with varying concentrations of VES for 24 h and cell survival was evaluated using the MTT assay. (B) Cell viability was evaluated by MTT assay and presented as the mean ± standard deviation compared with untreated control cells. *P<0.05 vs. 0 µM VES group. VES, vitamin E succinate.
Mentions: The effects of VES on the EC109 human esophageal cancer cell line was detected in the present study. The IC50 value of VES was determined by treating EC109 cells with increasing concentrations of VES for 24 h. IC50 value was calculated to be 25.1 µM for EC109 cells at 24 h (Fig. 1A). EC109 cells were treated with 10–100 µM VES for 24 h, and the cell viability was evaluated by MTT assay. The results demonstrated that the growth was decreased by ~45 and ~81% following treatment with 10 and 100 µM VES in EC109 cells (Fig. 1B). The current study also investigated whether the proliferation inhibition resulted from the induction of apoptosis in the cells.

Bottom Line: Furthermore, VES downregulated constitutively active basal levels of phosphorylated (p)‑serine‑threonine kinase AKT (AKT) and p‑mammalian target of rapamycin (mTOR), and decreased the phosphorylation of AKT substrates Bcl‑2‑associated death receptor and caspase‑9, in addition to mTOR effectors, ribosomal protein S6 kinase β1 and eIF4E‑binding protein 1.Phosphoinositide‑3‑kinase (PI3K) inhibitor, LY294002 suppressed p‑AKT and p‑mTOR, indicating PI3K is a common upstream mediator.Furthermore, the current study suggests that VES may be useful in a combinational therapeutic strategy employing an mTOR inhibitor.

View Article: PubMed Central - PubMed

Affiliation: Department of Thoracic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.

ABSTRACT
Esophageal cancer is the fourth most common gastrointestinal cancer, it generally has a poor prognosis and novel strategies are required for prevention and treatment. Vitamin E succinate (VES) is a potential chemical agent for cancer prevention and therapy as it exerts anti‑tumor effects in a variety of cancers. However, the role of VES in tumorigenesis and progression of cancer remains to be elucidated. The present study aimed to determine the effects of VES in regulating the survival and apoptosis of human esophageal cancer cells. EC109 human esophageal cancer cells were used to investigate the anti‑proliferative effects of VES. The MTT and Annexin V‑fluorescein isothiocyanate/propidium iodide assays demonstrated that VES inhibited cell proliferation and induced apoptosis in esophageal cancer cells. Furthermore, VES downregulated constitutively active basal levels of phosphorylated (p)‑serine‑threonine kinase AKT (AKT) and p‑mammalian target of rapamycin (mTOR), and decreased the phosphorylation of AKT substrates Bcl‑2‑associated death receptor and caspase‑9, in addition to mTOR effectors, ribosomal protein S6 kinase β1 and eIF4E‑binding protein 1. Phosphoinositide‑3‑kinase (PI3K) inhibitor, LY294002 suppressed p‑AKT and p‑mTOR, indicating PI3K is a common upstream mediator. The apoptosis induced by VES was increased by inhibition of AKT or mTOR with their respective inhibitor in esophageal cancer cells. The results of the present study suggested that VES targeted the PI3K/AKT signaling pathways and induced apoptosis in esophageal cancer cells. Furthermore, the current study suggests that VES may be useful in a combinational therapeutic strategy employing an mTOR inhibitor.

No MeSH data available.


Related in: MedlinePlus