Oncogenic micro RNAs versus Tumor-Suppressing Kinases LKB1/AMPK

As mentioned before, the majority of anti-PAK1 products such as CAPE and
curcumin are LKB1/AMPK activators. Thus, it is of great interest to find
any micro RNAs which control either LKB1 or AMPK, in addition to PAK1 per
se.

So far only one micro RNA has been identified by Sean Lawler's group
at OSU (Ohio State University) in 2010 (1) : it is called miRNA451.
This micro RNA is oncogenic and inactivates the tumor suppressive kinase LKB1
by down-regulating its activator "CAB39", a calcium-binding protein.
Since LKB1 directly inactivates PAK1 and activates AMPK, in theory
miRNA451 would activate PAK1, and inactivate AMPK.

So I wonder if anti-PAK1 products inactivate this micro RNA gene. So far nobody
has tested this notion directly. Interestingly, however, this miRNA is highly upregulated
in Schwannoma (2), an NF2 tumor in which PAK1 is abnormally activated,
due to the dysfunction of NF2 gene product (merlin) which is a direct inhibitor of PAK1.
Thus, it is almost certain that PAK1 up-regulates this miRNA.

Furthermore, high glucose level in glioma cells activates this gene, promoting their proliferation, whereas the low glucose level inactivates this gene blocking their growth. Thus, the promoter of this micro RNA gene somehow serves as a cellular glucose sensor.

So I trust that anti-PAK1 products (=AMPK activators) along with either CR (calorie restriction)/fast or vigorous exercise such as marathon would certainly inactivate this gene, leading to the cure of PAK1-dependent cancers/NF, the longevity and good health...

References:

1. Godlewski, J. et al (OSU). MicroRNA-451 Regulates LKB1/AMPK Signaling
and Allows Adaptation to Metabolic Stress in Glioma Cells. Mol. Cell, 2010,
37, 620-32.

2. Saydam, O. et al (MGH). miRNA-7 attenuation in schwannoma tumors stimulates
growth by upregulating three oncogenic signaling pathways. Cancer Res.
2010, in press.