Open AccessSp1king out cancer (….and fibrosis?)
Author(s) -
Leask Andrew
Publication year - 2012
Publication title -
journal of cell communication and signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 44
eISSN - 1873-961X
pISSN - 1873-9601
DOI - 10.1007/s12079-011-0147-x
Subject(s) - carcinogenesis , cancer , transcription factor , cancer research , fibrosis , sp1 transcription factor , medicine , bioinformatics , gene , biology , gene expression , promoter , genetics
Abstract It is becoming increasingly apparent that many of the basic mechanisms underlying cancers also underlie fibrotic diseases. For example, the Sp1 family of transcription factors plays an essential role in controlling the gene expression of proteins that promote both oncogenesis and fibrogenesis. The drug mithramycin, which prevents Sp1 binding to DNA, has been in use clinically for some cancers, but has side‐effects. However, other drugs exist that affect Sp1 activity through promoting Sp1 protein degradation. Evidence has emerged that low levels of mithramycin can be combined with these drugs to result in potent antitumorigenic effects without resulting in obvious toxicity (Gao et al. Cancer Res 2011 Jun 20; Jia et al. Cancer Res 70:1111‐1119, 2010). Given that Sp1 proteins also promote expression of profibrotic genes such as collagen type I and CCN2, it is possible that this combinatorial approach may be taken in the future to block not only cancer but also fibrosis.