Knocking down the expression of adenylate cyclase-associated protein 1 inhibits the proliferation and migration of breast cancer cells.

“Adenylate cyclase-associated protein 1 (CAP1) is a conserved protein that was found to be up-regulated in breast cancer and related to the migration of breast cancer…

CAP1 might be a potential molecular targeted therapy for surgery and immune treatment.”

http://www.ncbi.nlm.nih.gov/pubmed/24509166

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Upregulated expression of CAP1 is associated with tumor migration and metastasis in hepatocellular carcinoma.

“Hepatocellular carcinoma (HCC) is one of the most common cancers that exhibits high incidences of intrahepatic metastasis and tumor recurrence.

Adenylate cyclase-associated protein 1 (CAP1)… was recently reported to play a role in cell motility and the pathology of pancreatic cancer. In this study, we examined a potential role of CAP1 in HCC progression, and found that CAP1 was overexpressed in HCC specimens…

Collectively, our results indicated that upregulated expression of CAP1 might contribute heavily to the metastasis of HCC.”

http://www.ncbi.nlm.nih.gov/pubmed/24359721

 http://www.thctotalhealthcare.com/category/hepatocellular-carcinoma-hcc/

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Overexpression of adenylate cyclase-associated protein 1 is associated with metastasis of lung cancer.

“Lung cancer ranks first in both prevalence and mortality rates among all types of cancer. Metastasis is the main cause of treatment failure. Biomarkers are critical to early diagnosis and prediction and monitoring of progressive lesions…

The present study assessed the diagnostic and prognostic value of cyclase-associated protein 1 (CAP1) for lung cancer…

These findings suggest that overexpression of CAP1 in lung cancer cells, particularly at the metastatic stage, may have significant clinical implications as a diagnostic/prognostic factor for lung cancer.”

http://www.ncbi.nlm.nih.gov/pubmed/23842884

http://www.thctotalhealthcare.com/category/lung-cancer/

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Adenylate cyclase-associated protein 1 overexpressed in pancreatic cancers is involved in cancer cell motility

“Pancreatic cancer is a leading cause of cancer death worldwide… Pancreatic cancer has the worst prognosis among cancers due to the difficulty of early diagnosis and its aggressive behavior.

…the adenylate cyclase-associated protein 1 (CAP1) gene was shown to be overexpressed in all of the xenografts.

Knockdown of CAP1 by RNA interference resulted in the reduction of lamellipodium formation, motility, and invasion of pancreatic cancer cells.

This is the first report demonstrating the overexpression of CAP1 in pancreatic cancers and suggesting the involvement of CAP1 in the aggressive behavior of pancreatic cancer cells.”

http://www.nature.com/labinvest/journal/v89/n4/full/labinvest20095a.html

http://www.thctotalhealthcare.com/category/pancreatic-cancer/

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Inhibition of adenylate cyclase by delta 9-tetrahydrocannabinol in mouse spleen cells: a potential mechanism for cannabinoid-mediated immunosuppression.

“The ability of delta 9-Tetrahydrocannabinol (delta 9-THC) to modulate adenylate cyclase activity in mouse spleen cells was investigated…

delta 9-THC treated spleen cells demonstrated a 33% inhibition and a 66% inhibition in intracellular cAMP… respectively…

These studies suggest that inhibition of immune function by delta 9-THC may be mediated through the inhibition of intracellular cAMP early after antigen stimulation.”

http://www.ncbi.nlm.nih.gov/pubmed/1321935

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Anandamide, a naturally-occurring agonist of the cannabinoid receptor, blocks adenylate cyclase at the frog neuromuscular junction.

“Anandamide (arachydonylethanolamide) is a naturally-occurring ligand of the canabinoid receptor. When anandamide binds to its receptor, adenylate cyclase is inhibited…

The conclusions are that the motor nerve terminal has a cannabinoid receptor.

The binding of anandamide to this receptor seems to block adenylate cyclase.”

http://www.ncbi.nlm.nih.gov/pubmed/7953630

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The peripheral cannabinoid receptor: adenylate cyclase inhibition and G protein coupling.

“Two cannabinoid receptors, designated neuronal (or CB1) and peripheral (or CB2), have recently been cloned. Activation of CB1 receptors leads to inhibition of adenylate cyclase and N-type voltage-dependent Ca2+ channels.

Here we show, using a CB2 transfected Chinese hamster ovary cell line, that this receptor binds a variety of tricyclic cannabinoid ligands as well as the endogenous ligand anandamide.

Activation of the CB2 receptor by various tricyclic cannabinoids inhibits adenylate cyclase activity and this inhibition is pertussis toxin sensitive indicating that this receptor is coupled to the Gi/G(o) GTP-binding proteins…

These results characterize the CB2 receptor as a functional and distinctive member of the cannabinoid receptor family.”

http://www.ncbi.nlm.nih.gov/pubmed/7498464

 

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Nonclassical cannabinoid analgetics inhibit adenylate cyclase: development of a cannabinoid receptor model.

“Extensive structure-activity relationship studies have demonstrated that specific requirements within the cannabinoid structure are necessary to produce potent analgesia.

A three-point association between the agonist and the receptor mediating analgesia consists of: 1) the C ring hydroxyl, 2) the phenolic A ring hydroxyl, and 3) the A ring alkyl hydrophobic side chain. Potent tricyclic and bicyclic structures were synthesized as “nonclassical” cannabinoid analgetics that conform to this agonist-receptor three-point interaction model.

At the cellular level, centrally active cannabinoid drugs inhibit adenylate cyclase activity in a neuroblastoma cell line. The structure-activity relationship profile for inhibition of adenylate cyclase in vitro was consistent with this same three-point association of agonists with the receptor.

A correlation exists between the potency of drugs to produce analgesia in vivo and to inhibit adenylate cyclase in vitro.

Based on the parallels in structure-activity relationships and the enantioselective effects, it is postulated that the receptor that is associated with the regulation of adenylate cyclase in vitro may be the same receptor as that mediating analgesia in vivo.

A conceptualization of the cannabinoid analgetic receptor is presented.”

http://www.ncbi.nlm.nih.gov/pubmed/3352594

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Anandamide, a brain endogenous compound, interacts specifically with cannabinoid receptors and inhibits adenylate cyclase.

“A putative endogenous cannabinoid ligand, arachidonylethanolamide (termed “anandamide”), was isolated recently from porcine brain.

Here we demonstrate that this compound is a specific cannabinoid agonist and exerts its action directly via the cannabinoid receptors.

Anandamide specifically binds to membranes from cells transiently (COS) or stably (Chinese hamster ovary) transfected with an expression plasmid carrying the cannabinoid receptor DNA but not to membranes from control nontransfected cells.

Moreover, anandamide inhibited the forskolin-stimulated adenylate cyclase in the transfected cells and in cells that naturally express cannabinoid receptors (N18TG2 neuroblastoma) but not in control nontransfected cells. As with exogenous cannabinoids…

These data indicate that anandamide is an endogenous agonist that may serve as a genuine neurotransmitter for the cannabinoid receptor.”

http://www.ncbi.nlm.nih.gov/pubmed/8515284

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Regulation of adenylate cyclase by cannabinoid drugs. Insights based on thermodynamic studies.

“The abilities of lipophilic cannabinoid drugs to regulate adenylate cyclase activity in neuroblastoma cell membranes were analyzed by thermodynamic studies…

These data suggest that, for the entropy-driven hormone-stimulated adenylate cyclase enzyme, less disorder of the system occurs in the presence of regulators that inhibit the enzyme via Gi.

In summary, thermodynamic data suggest that cannabidiol can influence adenylate cyclase by increasing membrane fluidity, but that the inhibition of adenylate cyclase by delta 9-tetrahydrocannabinol is not related to membrane fluidization.”

http://www.ncbi.nlm.nih.gov/pubmed/2554920

“Regulation of adenylate cyclase in a cultured neuronal cell line by marijuana constituents, metabolites of delta-9-tetrahydrocannabinol, and synthetic analogs having psychoactivity.” http://www.ncbi.nlm.nih.gov/pubmed/2830535

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