임형신
2018-05-31T04:12:08Z
2018-05-31T04:12:08Z
2017-02
ARCHIVES OF PHARMACAL RESEARCH, v. 40, No. 2, Page. 146-151
0253-6269
1976-3786
https://link.springer.com/article/10.1007/s12272-016-0874-x
https://repository.hanyang.ac.kr/handle/20.500.11754/71767
The proteins p150(Sal2) (product of SALL2) and p53 share growth arrest and pro-apoptotic functions by independently inducing p21(Cip1/Waf1) and BAX, and both proteins are targeted by the human papilloma virus E6 protein, leading to blockage of growth arrest in infected cells. Loss of both p53 and Sall2 in mice causes significantly higher mortality and metastasis rates compared with p53 single mutant mice. Therefore, p150(Sal2) seems to have strong potential as a novel cancer biomarker for early diagnosis and risk prediction. Loss of SALL2 expression is observed in many cases of human serous ovarian carcinoma, whereas normal ovarian epithelial cells maintain high levels of the p150(Sal2) protein, supporting an important tumor suppressive role for p150(Sal2) in the human ovary. In contrast, p150(Sal2) is a transcription factor required to convert differentiated glioblastoma cells into stem-like tumor-propagating cells, suggesting that its functional roles are dependent on tissue types and cellular context. The function of p150(Sal2) in normal and diseased cells and possible therapeutic approaches are discussed in this review.
This work was supported by the National Science Foundation (to CKS; NSF CBET-1504174) and the research fund of Hanyang University (HY-2014-N) to HY.
en_US
PHARMACEUTICAL SOC KOREA
Ovarian carcinoma
Glioblastoma
Mouse polyomavirus
Human papillomavirus
p150(sal2)
p53
p21(Cip1/Waf1)
BAX
TUMOR-SUPPRESSOR GENE
EXPRESSION
TRANSCRIPTION
CANCER
ONCOGENE
PROMOTER
PROTEIN
CELLS
REGULATOR
Roles of SALL2 in tumorigenesis
Article
2
40
10.1007/s12272-016-0874-x
146-151
ARCHIVES OF PHARMACAL RESEARCH
Sung, Chang K
Yim, Hyungshin
2017007152
E
COLLEGE OF PHARMACY[E]
DEPARTMENT OF PHARMACY
hsyim