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Silencing SATB1 overcomes temozolomide resistance by downregulating MGMT expression and upregulating SLC22A18 expression in human glioblastoma cells
Blocking SATB1 may help overcome drug resistance by changing gene levels in human brain cancer cells
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Abstract
In recurrent glioblastoma tumors, SATB1 and MGMT protein levels are increased while SLC22A18 levels are decreased.
- Upregulation of SATB1 and MGMT, along with downregulation of SLC22A18, is associated with TMZ resistance in GBM U87 cells.
- Inactivation of SATB1 using shRNA leads to reduced MGMT expression and increased SLC22A18 expression in GBM cells.
- Immunohistochemical analysis shows a significant positive correlation between MGMT and SATB1 levels, and a negative correlation between SLC22A18 and SATB1 levels.
- In paired samples of recurrent and primary tumors, SATB1 and MGMT levels were higher in recurrent lesions, while SLC22A18 levels were lower.
- Knockdown of SATB1 enhances the effectiveness of TMZ in resistant GBM cells.
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