In this case, they continue to regenerate and re produce that can also spread to all other parts of the body organism. Khan, Mohammed I. et al. (2016) argue that ECS can control and regulate cancer.To start with, Michael Membrino of Neuro-Endocueticals, respectively maintains that Hemp Extract is the active component of cannabinoids. Similarly, they exist in the family of compounds that belong to different classes that can act on cannabinoid receptors CB1 and CB2. Furthermore, Khan, Mohammed I. et al. (2016) notes that cannabinoids are grouped into three classes, including synthetic cannabinoids, endocannabinoids, and phytocannabinoids. One way through which ECS regulate cancer is the fact that cancer is known characterized by uncontrolled cell division and cell death that originates from cumulative damage of significant regulatory genes (Guindon, & Hohmann, 2011).
In this case, the antiproliferative properties of hemp compounds (Δ9-THC) are used to inhibit lung adenocarcinoma cell growth. On the other hand, cannabinoids are known to induce synthesis of ceramides, which is comprised of fatty acids and sphingosine that are found in the cell membrane. The ceramides will lead to the activation of CB1 or CB2 receptor through the process of cell cycle arrest and apoptosis. In effect, the extracellular regulated kinase will promote apoptosis in the cancerous cell; therefore, regulating cancer (Guindon, & Hohmann, 2011). Additionally, the activation of CB1 and CB2 receptors stamps down adenylyl cyclase and reduce both cyclic adenosine monophosphate (cAMP) capacity and protein kinase A (PKA) activity. This action alone reduces the regulation of gene transcription leading to apoptosis.
Separately, it is argued that the cannabinoid receptors (CB1 and CB2) are upregulated in breast and prostate cancer. For instance, when the raised cannabinoids are combined with pro-apoptotic and antiproliferative capacities of the endocannabinoids, the chances of regulating cancer in high. In this case, when healthy cells are programmed in a manner to have the high capacity of developing more cannabinoid receptors when these cells become cancerous, they would be made more susceptible to the anti-cancer effects of the endocannabinoids.
Consequently, according to research conducted by Guindon, & Hohmann (2011) breast cancer is the malignant breast neoplasm. And when cannabinoids such as CB1 are expressed in the cells of the breast cancer will tend to show the anatomical distribution that is appropriate to regulate breast cancer proliferation. Moreover, in vitro research, it is noted that endocannabinoids and compound of cannabinoids are used to control the proliferation or migration, or apoptosis in various breast cancer situations.
The phytocannabinoids CBR is described as the class component of cannabinoids that usually stamps down cell proliferation, thereby increasing apoptosis and reduces migration in various lines of cancer cells. Separately, in vitro, research suggests that cannabinoids minimize tumor growth and metastasis together with cell development and angiogenesis in mice induced with various cancer cells (Guindon, & Hohmann, 2011).
For instance, Guindon, & Hohmann further explains that Δ9-THC have the ability to reduce the size of the tumor as well as lessen the number of tumor and lung metastases and stamps down both cell proliferation and angiogenesis. Suggestively, the vast majority of the research has agreed that phytocannabinoids and endocannabinoids have anti-cancer activity predominantly.
Separately, the research conducted by Guindon, & Hohmann (2011) indicates that the expression of the cannabinoid receptors (CB1) in different prostate cancer is associated with high immunoreactivity score.
Similarly, it was evident that CB1 expression is up-regulated in prostate cancer tissue. Conversely, CB2 receptors have also greater impact when expressed in different prostate cancer cell lines through the use of RT-PCR, immunofluorescence and Western blot.
In 2011, studies suggested that CB receptor expression in cancer cell will depend on the type of cancer. For example, an examination astrocytomas demonstrate that almost 70 percent of tumor expresses both CB1 or CB2 and the capacity to which CB2 expression correlated with the tumor malignancy (Hermanson, & Marnett, 2011). Besides, the activation of both CB receptors has shown to stimulate de novo synthesis of ceramide in human tumors comprising leukemia, pancreatic, glioma, and DLD-1 and HT29 colorectal cancer cells. Consequently, it has been indicated that hemp smokers have the ability to extract intake to the abolishment of the leukemia cancer cell in human patients.
On the other hand, looking at the lung cancer Cannabinoids tends to halt down the development of tumor without side effects (Chakravarti, Ravi, & Ganju, 2014). Also. Studies have indicated that for a patient with lung cancer, the participation of COX-2 and PPAR-γ in cannabinoids cause pro-apoptotic and tumor-regressive action. Additionally, the activation of CB1 or CB2 receptors expresses the apoptotic death of the tumorigenic epidermal cells thereby regulating skin cancer.
Looking at borne disease, Chakravarti, Ravi, & Ganju (2014) note that the skeletal endocannabinoid system plays a significant role in regulating bone cancer. In their explanation, they argue that the expressions of the levels of CB1 and CB2 receptors can attenuate pain and hyperalgesia in a metastatic bone patient.
Consequently, the CB1 receptor agonist arachidonoyl-2-chloroethylamine can generate antinociceptive properties when the intrathecal administration in this model is administered, which enhances the limb flinches and weight bearing.
In conclusion, Mike Membrino, President of Neuro-Endoneuticals presents that the available literature indicates that ECS is the target to suppress the evolution and progression of different types of cancer in the future disease management. Even though, this review focus on many types of cancer, endocannabinoids express various interesting effects that are dependent the tumor cells. Both synthetic cannabinoids and endocannabinoids systems are implicated in the stamping down cancer cell proliferation, and angiogenesis, which tends to reduce tumor development and growth and metastases and to induce apoptosis.
Chakravarti, B., Ravi, J., & Ganju, R. K. (2014). Cannabinoids as therapeutic agents in cancer: current status and future implications. Oncotarget, 5(15), 5852–5872.
Guindon, J., & Hohmann, A. G. (2011). The endocannabinoid system and cancer: therapeutic implications. British Journal of Pharmacology, 163(7), 1447–1463. http://doi.org/10.1111/j.1476-5381.2011.01327.x
Khan, M. I., Sobocińska, A. A., Czarnecka, A. M., Król, M., Botta, B., & Szczylik, C. (2016). The Therapeutic Aspects of the Endocannabinoid System (ECS) for Cancer and their Development: From Nature to Laboratory. Current Pharmaceutical Design, 22(12), 1756–1766. http://doi.org/10.2174/1381612822666151211094901
Hermanson, D. J., & Marnett, L. J. (2011). Cannabinoids, Endocannabinoids and Cancer. Cancer Metastasis Reviews, 30(3-4), 599–612. http://doi.org/10.1007/s10555-011-9318-8