573
Views
3
CrossRef citations to date
0
Altmetric
Cell Cycle News & Views

Switch of FANCL, a key FA-BRCA component, between tumor suppressor and promoter by alternative splicing

, &
Page 3356 | Published online: 23 Aug 2012

Figures & data

Figure 1. The wild-type (wt) of tumor suppressor genes exemplified by p53, Rb1 and FANCL can be switched to a different (d) form with oncogenic features, whereas the wt of canonical oncogenes, exemplified by k-ras and c-myc, are versatile or can be switched to a form with suppressive traits. The switch may occur via reversible mechanisms such as alternative (Alt.) transcription, splicing or translation, or via irreversible mechanisms such as mutation or partial deletion. Tumor-suppressive functions are typically manifested as enhanced (+) growth arrest, cell death or sensitivity to cancer treatments, whereas oncogenic traits include increased (+) proliferation, survival or resistance to therapies.

Figure 1. The wild-type (wt) of tumor suppressor genes exemplified by p53, Rb1 and FANCL can be switched to a different (d) form with oncogenic features, whereas the wt of canonical oncogenes, exemplified by k-ras and c-myc, are versatile or can be switched to a form with suppressive traits. The switch may occur via reversible mechanisms such as alternative (Alt.) transcription, splicing or translation, or via irreversible mechanisms such as mutation or partial deletion. Tumor-suppressive functions are typically manifested as enhanced (+) growth arrest, cell death or sensitivity to cancer treatments, whereas oncogenic traits include increased (+) proliferation, survival or resistance to therapies.