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Figure 3.6 The routes of signalling adopted by some miRNA to promote angiogenesis;
some activate angiogenic growth factors such as VEGF and bFGF suppress angiogenesis
inhibitors. Some transcription factors are also able to activate angiogenic miRNAs. References
are provided in the text. Hypoxia involves miRNAs in two ways. Hypoxia induces many
miRNAs, for example miRNAs-23, -24, -26, -27, -103, -107, -181, -210 and -213, some
via an HIF-dependent mechanism. HIF1-α activity is involved in some such as miRNA-210
to promote angiogenesis. Hypoxia induces miRNA-424 in an HIF-dependent manner and
promotes angiogenesis. It is said to reduce the expression of miRNA-34a with promotion of
EMT by targeting Notch signalling (Du et al., 2012). In contrast, miRNAs-221 and -222 seem
to downregulate c-Kit RTK and inhibit angiogenesis. There are some indications that mTOR
signalling might be inhibited by miRNA-100 leading to the inhibition of endothelial cell
proliferation and angiogenesis.
ANGIOGENESIS
miRNA-211
TSP-1
miRNA-194
miRNA-34a
P53
p21 miRNA-10
miRNA-211
EMT
miRNA-200c
mdm2
Bcl2/Bcl-xL/Bax
Cell
proliferation
Figure 3.7 p53/mdm2/bcl2-bax regulation of cell proliferation and apoptosis and the
modulation of signalling by miRNAs. The effects might occur as a consequence of altering
the balance of Bcl family pro- and anti-apoptosis genes. ER is also suggested as being able to
do this, but some reservations and caveats may be expressed in relation to that. References are
given in the text.
 
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