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Publication
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| Research Title |
STAT3 is a promising therapeutic target for cholagiocarcinoma with hyperglycemia |
| Date of Distribution |
10 January 2016 |
| Conference |
| Title of the Conference |
Keystone Symposia-Cytokine JAK-STAT in Immunity and Disease |
| Organiser |
Keystone Symposia |
| Conference Place |
Sheraton Steamboat Resort, Steamboat Springs |
| Province/State |
Corolado |
| Conference Date |
10 January 2016 |
| To |
15 January 2016 |
| Proceeding Paper |
| Volume |
- |
| Issue |
- |
| Page |
51 |
| Editors/edition/publisher |
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| Abstract |
The incidence of cholangiocarcinoma (CCA), a bile duct malignancy, is high in the northeastern Thailand and is now globally increasing. Diabetes Mellitus (DM) is a well-documented risk factor for CCA development, however, its effect on CCA progression is still unclear. Attempting to clarify the effect of high glucose on CCA progression, two CCA cell lines; KKU-213 and KKU-214, were cultured in normal and high glucose medium and compared. The results demonstrated that cells in high glucose condition had increased progressive phenotypes—namely proliferation, adhesion, migration and invasion. The underlying mechanism using phosphokinase array indicated STAT3 as a candidate pathway. STAT3 activation in high glucose condition was verified using immunoblotting and immunocytofluorescent staining. The results indicated that high glucose condition increased STAT3 phosphorylation and nuclear localization, resulting in upregulation of STAT3 downstream targeted genes that related to progressive phenotypes. The immunohistochemistry of CCA tissues from patients with hyperglycemia revealed significantly higher nuclear STAT3 expression (P <0.05) than those with normal blood glucose. Moreover, the level of STAT3 expression was corresponded to the level of fasting blood glucose of the patients (P = 0.001). Furthermore, either controlling glucose level or using STAT3 inhibitor can reduce STAT3 activation in high glucose condition, resulting in reduced proliferation of CCA cells. In summary, STAT3 is responsible for high glucose induced CCA progression and controlling glucose level or inhibiting STAT3 action are the alternative therapeutic approaches for CCA patients with DM. |
| Author |
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| Peer Review Status |
มีผู้ประเมินอิสระ |
| Level of Conference |
นานาชาติ |
| Type of Proceeding |
Abstract |
| Type of Presentation |
Poster |
| Part of thesis |
true |
| Presentation awarding |
false |
| Attach file |
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| Citation |
0
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Journal Publication
ไทย