Cannabis is healing humans suffering from cancer.
International Journal of Cancer
November 2007
The cannabinoid δ9-tetrahydrocannabinol inhibits RAS-MAPK and PI3K-AKT survival signalling and induces BAD-mediated apoptosis in colorectal cancer cells
Abstract
Deregulation of cell survival pathways and resistance to apoptosis are widely accepted to be fundamental aspects of tumorigenesis.
As in many tumours, the aberrant growth and survival of colorectal tumour cells is dependent upon a small number of highly activated signalling pathways, the inhibition of which elicits potent growth inhibitory or apoptotic responses in tumour cells.
Accordingly, there is considerable interest in therapeutics that can modulate survival signalling pathways and target cancer cells for death.
There is emerging evidence that cannabinoids, especially Δ9-tetrahydrocannabinol (THC), may represent novel anticancer agents, due to their ability to regulate signalling pathways critical for cell growth and survival.
Here, we report that CB1 and CB2 cannabinoid receptors are expressed in human colorectal adenoma and carcinoma cells, and show for the first time that THC induces apoptosis in colorectal cancer cells. …
These data suggest an important role for CB1 receptors and BAD in the regulation of apoptosis in colorectal cancer cells.
The use of THC, or selective targeting of the CB1 receptor, may represent a novel strategy for colorectal cancer therapy.
The cannabinoid []9-tetrahydrocannabinol inhibits RAS-MAPK and PI3K-AKT survival signalling and induces BAD-mediated apoptosis in colorectal cancer cells – Greenhough – 2007 – International Journal of Cancer – Wiley Online Library
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Clinical Cancer Research
December 2008
Cannabinoid Receptor Activation Induces Apoptosis through Tumor Necrosis Factor α–Mediated Ceramide De novo Synthesis in Colon Cancer Cells
Abstract
Purpose:
Cannabinoids have been recently proposed as a new family of potential antitumor agents.
The present study was undertaken to investigate the expression of the two cannabinoid receptors, CB1 and CB2, in colorectal cancer and to provide new insight into the molecular pathways underlying the apoptotic activity induced by their activation.
Experimental Design:
Cannabinoid receptor expression was investigated in both human cancer specimens and in the … colon cancer cell lines.
The effects of the CB1 agonist … on tumor cell apoptosis and ceramide and tumor necrosis factor (TNF)-α production were evaluated.
Results:
We show that the CB1 receptor was mainly expressed in human normal colonic epithelium whereas tumor tissue was strongly positive for the CB2 receptor.
The activation of the CB1 and, more efficiently, of the CB2 receptors induced apoptosis and increased ceramide levels in the … cells.
The CB2 agonist … also reduced the growth of … cells in a mouse model of colon cancer.
Conclusions:
The present study shows that either CB1 or CB2 receptor activation induces apoptosis through ceramide de novo synthesis in colon cancer cells. …
Cannabinoid Receptor Activation Induces Apoptosis through Tumor Necrosis Factor ??Mediated Ceramide De novo Synthesis in Colon Cancer Cells
———————————————————-
Pharmacological Research
August 2009
Cannabinoids in intestinal inflammation and cancer
Abstract
Emerging evidence suggests that cannabinoids may exert beneficial effects in intestinal inflammation and cancer. Adaptive changes of the endocannabinoid system have been observed in intestinal biopsies from patients with inflammatory bowel disease and colon cancer.
Studies on epithelial cells have shown that cannabinoids exert antiproliferative, antimetastatic and apoptotic effects as well as reducing cytokine release and promoting wound healing.
In vivo, cannabinoids – via direct or indirect activation of CB1 and/or CB2 receptors – exert protective effects in well-established models of intestinal inflammation and colon cancer.
Pharmacological elevation of endocannabinoid levels may be a promising strategy to counteract intestinal inflammation and colon cancer.
Cannabinoids in intestinal inflammation and cancer
————————————————————-
Journal of Molecular Medicine
August 2012
Chemopreventive effect of the non-psychotropic phytocannabinoid cannabidiol on experimental colon cancer
Abstract
Colon cancer affects millions of individuals in Western countries.
Cannabidiol, a safe and non-psychotropic ingredient of Cannabis sativa, exerts pharmacological actions (antioxidant and intestinal antinflammatory) and mechanisms (inhibition of endocannabinoid enzymatic degradation) potentially beneficial for colon carcinogenesis.
Thus, we investigated its possible chemopreventive effect in the model of colon cancer …
Cannabidiol-reduced ACF, polyps and tumours …
In colorectal carcinoma cell lines, cannabidiol protected DNA from oxidative damage, increased endocannabinoid levels and reduced cell proliferation …
It is concluded that cannabidiol exerts chemopreventive effect in vivo and reduces cell proliferation through multiple mechanisms.
Chemopreventive effect of the non-psychotropic phytocannabinoid cannabidiol on experimental colon cancer – Springer
————————————————————–
Phytomedicine: International Journal of Phytotherapy and Phytopharmacology
December 27, 2013
Inhibition of colon carcinogenesis by a standardized Cannabis sativa extract with high content of cannabidiol
Abstract
Purpose:
Colon cancer is a major public health problem.
Cannabis-based medicines are useful adjunctive treatments in cancer patients.
Here, we have investigated the effect of a standardized Cannabis sativa extract with high content of cannabidiol (CBD), here named CBD BDS, i.e. CBD botanical drug substance, on colorectal cancer cell proliferation and in experimental models of colon cancer in vivo.
Methods:
Proliferation was evaluated in colorectal carcinoma … as well as in healthy colonic cells …
CBD BDS binding was evaluated by its ability to displace [3H]CP55940 from human cannabinoid CB1 and CB2 receptors.
In vivo, the effect of CBD BDS was examined on the preneoplastic lesions (aberrant crypt foci), polyps and tumours induced by the carcinogenic agent azoxymethane (AOM) as well as in a xenograft model of colon cancer in mice.
Results:
CBD BDS and CBD reduced cell proliferation in tumoral, but not in healthy, cells.
The effect of CBD BDS was counteracted by selective CB1 and CB2 receptor antagonists.
Pure CBD reduced cell proliferation in a CB1-sensitive antagonist manner only.
In binding assays, CBD BDS showed greater affinity than pure CBD for both CB1 and CB2 receptors, with pure CBD having very little affinity.
In vivo, CBD BDS reduced AOM-induced preneoplastic lesions and polyps as well as tumour growth in the xenograft model of colon cancer.
Conclusions:
CBD BDS [Cannabidiol Botanical Drug Substance] attenuates colon carcinogenesis and inhibits colorectal cancer cell proliferation via CB1 and CB2 receptor activation.
The results may have some clinical relevance for the use of Cannabis-based medicines in cancer patients.
Elsevier
——————————————————————-
In Vitro Cellular and Developmental Biology – Animal
January 2014
Physiological intestinal oxygen modulates the Caco-2 cell model and increases sensitivity to the phytocannabinoid cannabidiol
Abstract
The Caco-2 cell model is widely used as a model of colon cancer and small intestinal epithelium but, like most cell models, is cultured in atmospheric oxygen conditions (∼21%).
This does not reflect the physiological oxygen range found in the colon.
In this study, we investigated the effect of adapting the Caco-2 cell line to routine culturing in a physiological oxygen (5%) environment.
Under these conditions, cells maintain a number of key characteristics of the Caco-2 model, such as increased formation of tight junctions and alkaline phosphatase expression over the differentiation period and maintenance of barrier function.
However, these cells exhibit differential oxidative metabolism, proliferate less and become larger during differentiation.
In addition, these cells were more sensitive to cannabidiol-induced antiproliferative actions through changes in cellular energetics: from a drop of oxygen consumption rate and loss of mitochondrial membrane integrity in cells treated under atmospheric conditions to an increase in reactive oxygen species in intact mitochondria in cells treated under low-oxygen conditions.
Inclusion of an additional physiological parameter, sodium butyrate, into the medium revealed a cannabidiol-induced proliferative response at low doses.
These effects could impact on its development as an anticancer therapeutic, but overall, the data supports the principle that culturing cells in microenvironments that more closely mimic the in vivo conditions is important for drug screening and mechanism of action studies.
Physiological intestinal oxygen modulates the Caco-2 cell model and increases sensitivity to the phytocannabinoid cannabidiol – Springer
Source : http://www.welovetheherb.com/pictures/colon-cancer-cannabis-studies.html
International Journal of Cancer
November 2007
The cannabinoid δ9-tetrahydrocannabinol inhibits RAS-MAPK and PI3K-AKT survival signalling and induces BAD-mediated apoptosis in colorectal cancer cells
Abstract
Deregulation of cell survival pathways and resistance to apoptosis are widely accepted to be fundamental aspects of tumorigenesis.
As in many tumours, the aberrant growth and survival of colorectal tumour cells is dependent upon a small number of highly activated signalling pathways, the inhibition of which elicits potent growth inhibitory or apoptotic responses in tumour cells.
Accordingly, there is considerable interest in therapeutics that can modulate survival signalling pathways and target cancer cells for death.
There is emerging evidence that cannabinoids, especially Δ9-tetrahydrocannabinol (THC), may represent novel anticancer agents, due to their ability to regulate signalling pathways critical for cell growth and survival.
Here, we report that CB1 and CB2 cannabinoid receptors are expressed in human colorectal adenoma and carcinoma cells, and show for the first time that THC induces apoptosis in colorectal cancer cells. …
These data suggest an important role for CB1 receptors and BAD in the regulation of apoptosis in colorectal cancer cells.
The use of THC, or selective targeting of the CB1 receptor, may represent a novel strategy for colorectal cancer therapy.
The cannabinoid []9-tetrahydrocannabinol inhibits RAS-MAPK and PI3K-AKT survival signalling and induces BAD-mediated apoptosis in colorectal cancer cells – Greenhough – 2007 – International Journal of Cancer – Wiley Online Library
——————————————————————
Clinical Cancer Research
December 2008
Cannabinoid Receptor Activation Induces Apoptosis through Tumor Necrosis Factor α–Mediated Ceramide De novo Synthesis in Colon Cancer Cells
Abstract
Purpose:
Cannabinoids have been recently proposed as a new family of potential antitumor agents.
The present study was undertaken to investigate the expression of the two cannabinoid receptors, CB1 and CB2, in colorectal cancer and to provide new insight into the molecular pathways underlying the apoptotic activity induced by their activation.
Experimental Design:
Cannabinoid receptor expression was investigated in both human cancer specimens and in the … colon cancer cell lines.
The effects of the CB1 agonist … on tumor cell apoptosis and ceramide and tumor necrosis factor (TNF)-α production were evaluated.
Results:
We show that the CB1 receptor was mainly expressed in human normal colonic epithelium whereas tumor tissue was strongly positive for the CB2 receptor.
The activation of the CB1 and, more efficiently, of the CB2 receptors induced apoptosis and increased ceramide levels in the … cells.
The CB2 agonist … also reduced the growth of … cells in a mouse model of colon cancer.
Conclusions:
The present study shows that either CB1 or CB2 receptor activation induces apoptosis through ceramide de novo synthesis in colon cancer cells. …
Cannabinoid Receptor Activation Induces Apoptosis through Tumor Necrosis Factor ??Mediated Ceramide De novo Synthesis in Colon Cancer Cells
———————————————————-
Pharmacological Research
August 2009
Cannabinoids in intestinal inflammation and cancer
Abstract
Emerging evidence suggests that cannabinoids may exert beneficial effects in intestinal inflammation and cancer. Adaptive changes of the endocannabinoid system have been observed in intestinal biopsies from patients with inflammatory bowel disease and colon cancer.
Studies on epithelial cells have shown that cannabinoids exert antiproliferative, antimetastatic and apoptotic effects as well as reducing cytokine release and promoting wound healing.
In vivo, cannabinoids – via direct or indirect activation of CB1 and/or CB2 receptors – exert protective effects in well-established models of intestinal inflammation and colon cancer.
Pharmacological elevation of endocannabinoid levels may be a promising strategy to counteract intestinal inflammation and colon cancer.
Cannabinoids in intestinal inflammation and cancer
————————————————————-
Journal of Molecular Medicine
August 2012
Chemopreventive effect of the non-psychotropic phytocannabinoid cannabidiol on experimental colon cancer
Abstract
Colon cancer affects millions of individuals in Western countries.
Cannabidiol, a safe and non-psychotropic ingredient of Cannabis sativa, exerts pharmacological actions (antioxidant and intestinal antinflammatory) and mechanisms (inhibition of endocannabinoid enzymatic degradation) potentially beneficial for colon carcinogenesis.
Thus, we investigated its possible chemopreventive effect in the model of colon cancer …
Cannabidiol-reduced ACF, polyps and tumours …
In colorectal carcinoma cell lines, cannabidiol protected DNA from oxidative damage, increased endocannabinoid levels and reduced cell proliferation …
It is concluded that cannabidiol exerts chemopreventive effect in vivo and reduces cell proliferation through multiple mechanisms.
Chemopreventive effect of the non-psychotropic phytocannabinoid cannabidiol on experimental colon cancer – Springer
————————————————————–
Phytomedicine: International Journal of Phytotherapy and Phytopharmacology
December 27, 2013
Inhibition of colon carcinogenesis by a standardized Cannabis sativa extract with high content of cannabidiol
Abstract
Purpose:
Colon cancer is a major public health problem.
Cannabis-based medicines are useful adjunctive treatments in cancer patients.
Here, we have investigated the effect of a standardized Cannabis sativa extract with high content of cannabidiol (CBD), here named CBD BDS, i.e. CBD botanical drug substance, on colorectal cancer cell proliferation and in experimental models of colon cancer in vivo.
Methods:
Proliferation was evaluated in colorectal carcinoma … as well as in healthy colonic cells …
CBD BDS binding was evaluated by its ability to displace [3H]CP55940 from human cannabinoid CB1 and CB2 receptors.
In vivo, the effect of CBD BDS was examined on the preneoplastic lesions (aberrant crypt foci), polyps and tumours induced by the carcinogenic agent azoxymethane (AOM) as well as in a xenograft model of colon cancer in mice.
Results:
CBD BDS and CBD reduced cell proliferation in tumoral, but not in healthy, cells.
The effect of CBD BDS was counteracted by selective CB1 and CB2 receptor antagonists.
Pure CBD reduced cell proliferation in a CB1-sensitive antagonist manner only.
In binding assays, CBD BDS showed greater affinity than pure CBD for both CB1 and CB2 receptors, with pure CBD having very little affinity.
In vivo, CBD BDS reduced AOM-induced preneoplastic lesions and polyps as well as tumour growth in the xenograft model of colon cancer.
Conclusions:
CBD BDS [Cannabidiol Botanical Drug Substance] attenuates colon carcinogenesis and inhibits colorectal cancer cell proliferation via CB1 and CB2 receptor activation.
The results may have some clinical relevance for the use of Cannabis-based medicines in cancer patients.
Elsevier
——————————————————————-
In Vitro Cellular and Developmental Biology – Animal
January 2014
Physiological intestinal oxygen modulates the Caco-2 cell model and increases sensitivity to the phytocannabinoid cannabidiol
Abstract
The Caco-2 cell model is widely used as a model of colon cancer and small intestinal epithelium but, like most cell models, is cultured in atmospheric oxygen conditions (∼21%).
This does not reflect the physiological oxygen range found in the colon.
In this study, we investigated the effect of adapting the Caco-2 cell line to routine culturing in a physiological oxygen (5%) environment.
Under these conditions, cells maintain a number of key characteristics of the Caco-2 model, such as increased formation of tight junctions and alkaline phosphatase expression over the differentiation period and maintenance of barrier function.
However, these cells exhibit differential oxidative metabolism, proliferate less and become larger during differentiation.
In addition, these cells were more sensitive to cannabidiol-induced antiproliferative actions through changes in cellular energetics: from a drop of oxygen consumption rate and loss of mitochondrial membrane integrity in cells treated under atmospheric conditions to an increase in reactive oxygen species in intact mitochondria in cells treated under low-oxygen conditions.
Inclusion of an additional physiological parameter, sodium butyrate, into the medium revealed a cannabidiol-induced proliferative response at low doses.
These effects could impact on its development as an anticancer therapeutic, but overall, the data supports the principle that culturing cells in microenvironments that more closely mimic the in vivo conditions is important for drug screening and mechanism of action studies.
Physiological intestinal oxygen modulates the Caco-2 cell model and increases sensitivity to the phytocannabinoid cannabidiol – Springer
Source : http://www.welovetheherb.com/pictures/colon-cancer-cannabis-studies.html
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