MACF1 knockdown in glioblastoma multiforme cells increases temozolomide-induced cytotoxicity.
- Author:
Si-di XIE
1
;
Zi-Yang CHEN
;
Hai WANG
;
Min-Yi HE
;
Yun-Tao LU
;
Bing-Xi LEI
;
He-Zhen LI
;
Ya-Wei LIU
;
Song-Tao QI
Author Information
- Publication Type:Journal Article
- From: Journal of Southern Medical University 2017;37(9):1183-1189
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of microtubule-actin crosslinking factor 1 (MACF1) in the response of glioma cells to temozolomide (TMZ).
METHODSTMZ was applied to a human gliomablastoma cell line (U87) and changes in the protein expression and cellular localization were determined with Western blot, RT-PCR, and immunofluorescence. The responses of the cells with MACF1 expression knockdown by RNA interference to TMZ were assessed. TMZ-induced effects on MACF1 expression were also assessed by immunohistochemistry in a nude mouse model bearing human glioblastoma xenografts.
RESULTSTMZ resulted in significantly increased MACF1 expression (by about 2 folds) and changes in its localization in the gliomablastoma cells both in vitro and in vivo (P<0.01). Knockdown of MACF1 reduced the proliferation (by 45%) of human glioma cell lines treated with TMZ (P<0.01). TMZ-induced changes in MACF1 expression was accompanied by cytoskeletal rearrangement.
CONCLUSIONMACF1 may be a potential therapeutic target for glioblastoma.