Natural EGFR inhibitors?

[al from Canada]

Isn't olive oil (oleic acid) an ERB2 inhibiotr?

Al

[michele u]

Does anyone know if taking Flaxseed oil capsules that have 180mg of oleic acid and linoleic acid would do the same thing as taking olive oil? Olive oil is nasty and it has alot of calories in it. Not saying that i won't take it if i have to, but it's expensive too!

[al from Canada]

Hi Michelle,
That's what I give Linda and I cook exclusively with olive oil.

Take care,
Al

The omega three six balance has been reported in trials as impacting on ErbB-2 expression in murine trials. The more I read the more I am convinced at a very amateur level that if you do nothing else at a dietary level it is importatant to try and balance the omega threes and sixes. Fats are fundamental to all life and according to literature on the subject played a large part in evolution or intelligent design which ever you choose.

Flax seed and olive oil are very different, have different constituents and are reported in general terms as being potentially benificial for different reasons. There may be common ground in that they both impact on the lipd pathways, and I would guess have a lot of interactive effects.

Fish oil is a strong recommendation to.

There are lots of posts on this site if you do a searches on omega three, olive oil, fish oil etc.

RB

This is useful link I found that clarifies the differences between EFGR and ErbB -2.

I will keep an eye out for specific links between ErbB -1 (EFGR) and omega three nine olive oil etc.


RB


http://www.iressa.com/iressaHCP/9898_12803_5_1_0.aspx

ABSTRACT

The EGFR family and intracellular signalling
The EGFR is part of a subfamily of four closely related receptors:

* EGFR (ErbB-1)
* Her 2/neu (ErbB-2)
* Her 3 (ErbB-3)
* Her 4 (ErbB-4)

Increased EGFR-mediated signalling can contribute to a cell moving into a state of continuous, uncontrolled cell division; expanding the population of malignant cells and increasing the tumour mass.

The processes by which this occurs begins when the receptors, which are inactive single units or monomers, become activated by the binding of the appropriate ligand.

This causes the receptors to pair together forming a dimer. The dimers may be formed either from two identical receptors, for example the EGF-1 receptor (EGFR) can pair with another EGFR-1 receptor to form a homodimer; or from two non-identical receptors, for example an EGFR can pair with a different receptor such as Her2/neu, forming an asymmetrical homodimer.

The pairing of the receptors activates the tyrosine kinase enzyme located in the intracellular domain of the receptor. This causes both intracellular domains to become transphosphorylated, which, in turn, initiates a cascade of events that eventually results in the signal reaching the nucleus [1] .

The sequence of events that occur when the EGFR becomes activated, leading to the cell moving into a state of continuous, uncontrolled division are as follows:

1. Activated EGFR recruits a number of proteins from the cytoplasm to form a linked complex.
2. Interactions between these proteins leads to the activation of a protein called ras.
3. Activated ras protein initiates a cascade of phosphorylations
4. Phosphorylation cascade activates mitogen activated protein kinase (MAPK)
5. MAP kinase delivers the signal from the cytoplasm to the nucleus
6. Signal reaches nucleus and triggers an accumulation of cyclin D
7. In association with cyclin-dependent kinases (cdks), cyclin D forces the cell to move into the active phase of division [2].


Models of ligand-receptor interactions were traditionally thought of as linear pathways of intracellular signals that link receptor activation to a single cell response. However, we now know that membrane receptor activation results in a number highly complex events in which several pathways are regulated simultaneous [3] .

EGFR is also involved in other processes crucial to tumour progression: apoptosis, angiogenesis and metastasis.


Back to top


References

1. Wells A. Molecules in focus EGF receptor. International Journal of Biochemistry and Cell Biology, 1999;31:637-643.
2. Lundberg AS, Weinberg RA Control of the cell cycle and apoptosis. European Journal of Cancer, 1999;35:1886-1894.
3. Brugge JS, McCormick F. Cell regulation intracellular networking. Current Opinion in Cell Biology, 1999;11:173-176.