14-3-3ζ protein mediates gemcitabine resistance in NK/T-cell lymphoma / 中华血液学杂志
Chinese Journal of Hematology
; (12): 906-911, 2019.
Article
ي Zh
| WPRIM
| ID: wpr-1012094
المكتبة المسؤولة:
WPRO
ABSTRACT
Objective:
To explore the molecular mechanisms of 14-3-3ζ in gemcitabine resistance in extranodal NK/T-cell lymphoma, nasal type (ENKTL) .Methods:
The effects of cell proliferation and invasion were detected by cell counting kit-8 (CCK-8) assay and transwell assay. YTS cells were exposed to gradually increased concentrations of gemcitabine to establish gemcitabine-resistant YTS cells (YTS-gem) in vitro. 14-3-3ζ specific siRNA lentiviral vector was transfected into YTS and YTS-gem cells to downregulate 14-3-3ζ expression, and stable transfected cell clones were screened. The protein expression was determined by Western blot.Results:
①14-3-3ζ expression was significantly up-regulated in gemcitabine resistant YTS-gem cells, comparing with that of YTS cells (P<0.05) . ②The results of CCK-8 and transwell assay showed that downregulation of 14-3-3ζ significantly reduced the cell proliferation and invasion abilities (P<0.05) . ③Downregulation of 14-3-3ζ could restore gemcitabine sensitivity in gemcitabine resistant YTS-gem cells (P<0.05) . ④Western blotting results showed that knockdown of 14-3-3ζ significantly upregulated pro-apoptotic Bax, and downregulated anti-apoptotic Bcl-2, Caspase-3, cleaved caspase-3, Cyclin D1 in gemcitabine-resistant YTS-gem cells (P<0.05) . There was no significant difference in p53 ang P-gp expression levels.Conclusions:
14-3-3ζ was upregulated in gemcitabine resistant YTS cells. Overexpression of 14-3-3ζ promoted cell proliferation and enhanced cell migration. 14-3-3ζ contributed to gemcitabine resistance to ENKTL through anti-apoptosis.Key words
النص الكامل:
1
الفهرس:
WPRIM
الموضوع الرئيسي:
Drug Resistance, Neoplasm
/
Cell Line, Tumor
/
Deoxycytidine
/
14-3-3 Proteins
/
Lymphoma, Extranodal NK-T-Cell
/
Gemcitabine
المحددات:
Humans
اللغة:
Zh
مجلة:
Chinese Journal of Hematology
السنة:
2019
نوع:
Article