Important -- GABA and Colon Cancer -- Expert advice needed

[Guest guest]

I was looking up GABA and Gabapentin in regards to trying to get some

help with my neuropathy. I thought it might be a good idea to check

whether there were any issues regarding GABA and cancer, and I got

several hits regarding the exact type of cancer I have -- colon

cancer.

Apparently colon cancer cells are massively studded with GABA

receptors! They don't know why. The only other type of cancer that

comes close is ovarian cancer, which also shows an overload of GABA

receptors.

At any rate, the GABA agonist Nembutol apparently significantly

slows down the metastasis of colon cancer by affecting the GABA

receptors. The downside of this drug, of course, is that it is an

exceptionally powerful barbituate.

Now, my question is this -- doesn't an " agonist " fire up the

receptors it " agonizes " ? If so, wouldn't large doses of GABA itself

do the same thing, or something similar, without the side effects?

Similarly, would gabapentin, which mimics GABA, do a similar thing?

Or would taking extra GABA cause the colon cancer to EXPLODE??? Why

would colon cancer have massive amounts of GABA receptors except to

help the darned cells proliferate?

I'm not at all sure on this -- any input would be helpful. The

information about GABA and colon cancer comes from JUST ONE STUDY in

2004, but this study seems to have been discussed repeatedly over the

last 4 years, even though it has never been replicated.

If anyone wants to google " GABA " and " colon cancer " you will pick up

a link to this report immediately.

[Guest guest]

I am not an expert,sorry, and I am wondering if these gaba receptors

involved in colon cancer were GABA A or GABA B...

in prostate cancer it seemed relevant...

karla

Gamma-aminobutyric acid as a promoting factor of cancer metastasis;

induction of matrix metalloproteinase production is potentially its

underlying mechanism.

Azuma H, Inamoto T, Sakamoto T, Kiyama S, Ubai T, Shinohara Y,

Maemura K, Tsuji M, Segawa N, Masuda H, Takahara K, Katsuoka Y,

Watanabe M.

Departments of Urology, Osaka Medical College, Takatsuki, Osaka,

Japan.

We investigated expression of gamma-aminobutyric acid (GABA),

glutamate decarboxylase, and matrix metalloproteinase (MMP) in the

prostates of patients with cancer or benign prostatic hypertrophy by

immunohistochemical study. Marked expression of GABA, glutamate

decarboxylase 67, and MMPs was observed in the prostates of cancer

patients with metastasis (n = 72) and lymph node metastasis, although

only sparse expression was noted in those of cancer patients without

metastasis (n = 76) or patients with benign prostatic hypertrophy (n

= 152). We then investigated the influence of GABA stimulation on in

vitro MMP production and the invasive ability of cancer cells using

human prostate cancer cell line C4-2. The production of MMPs

increased significantly in cancer cells after a 24-h incubation with

GABA. Cell invasion assay using a BioCoat Matrigel Invasion Chamber

kit revealed that GABA stimulation significantly promoted the

invasive ability of cancer cells and that addition of MMP inhibitor

GM6001 significantly decreased GABA-induced migration. This may

indicate the involvement of MMP activity in GABA-induced cancer cell

invasion. We further analyzed the transmission pathway by performing

GABA receptor modulation. The GABA( receptor agonist baclofen

significantly increased MMP production as well as invasive ability.

Moreover, blockade of the GABA( receptor pathway using GABA(

receptor antagonist CGP 35348 significantly inhibited GABA-induced

MMP production and invasive ability in cancer cells, whereas GABA(A)

receptor modulation did not influence MMP production or the invasive

ability of cancer cells. Thus, increased expression of GABA may be

implicated in cancer metastasis by promoting MMP production in cancer

cells, and the GABA( receptor pathway may be involved in the

process.

PMID: 14678958 [PubMed - indexed for MEDLINE

..

-

[Guest guest]

Jim,

A receptor AGONIST causes an effect directly on a receptor. This effect

can be to either increase or decrease activity.

A receptor ANTAGONIST simple attaches to the receptor without directly

affecting its activity. It can have an indirect effect by blocking agonists.

In the case you referenced, Nembutol, a GABA receptor agonist, attaches

to the GABA site and causes an effect opposite to GABA.

GABA would stimulate cell proliferation in cells with GABA receptors.

Mike

jrrjim wrote:

>

> I was looking up GABA and Gabapentin in regards to trying to get some

> help with my neuropathy. I thought it might be a good idea to check

> whether there were any issues regarding GABA and cancer, and I got

> several hits regarding the exact type of cancer I have -- colon

> cancer.

>

> Apparently colon cancer cells are massively studded with GABA

> receptors! They don't know why. The only other type of cancer that

> comes close is ovarian cancer, which also shows an overload of GABA

> receptors.

>

> At any rate, the GABA agonist Nembutol apparently significantly

> slows down the metastasis of colon cancer by affecting the GABA

> receptors. The downside of this drug, of course, is that it is an

> exceptionally powerful barbituate.

>

> Now, my question is this -- doesn't an " agonist " fire up the

> receptors it " agonizes " ? If so, wouldn't large doses of GABA itself

> do the same thing, or something similar, without the side effects?

> Similarly, would gabapentin, which mimics GABA, do a similar thing?

>

> Or would taking extra GABA cause the colon cancer to EXPLODE??? Why

> would colon cancer have massive amounts of GABA receptors except to

> help the darned cells proliferate?

>

> I'm not at all sure on this -- any input would be helpful. The

> information about GABA and colon cancer comes from JUST ONE STUDY in

> 2004, but this study seems to have been discussed repeatedly over the

> last 4 years, even though it has never been replicated.

>

> If anyone wants to google " GABA " and " colon cancer " you will pick up

> a link to this report immediately.

>

>

[Guest guest]

>

> Jim,

>

> A receptor AGONIST causes an effect directly on a receptor. This

effect

> can be to either increase or decrease activity.

> A receptor ANTAGONIST simple attaches to the receptor without

directly

> affecting its activity. It can have an indirect effect by blocking

agonists.

> In the case you referenced, Nembutol, a GABA receptor agonist,

attaches

> to the GABA site and causes an effect opposite to GABA.

> GABA would stimulate cell proliferation in cells with GABA

receptors.

>

> Mike

>