Lung cancer patient SHRUNK tumour 'using cannabidiol CBD oil'. CANNABIS CBD oil more than halved the size of a man's tumour. Using CBD/THC Oil to fight metastatic lung cancer. Posted by @lighthouse68, Aug 10, I am looking for suggested starting dosage information. Liked by. Keywords: Cancer, Cannabidiol, Cannabinoids, Cannabis, CBD, .. against cancer in murine lung cancer model (Lewis lung carcinoma, 3LL.
Lung Cannabidiol (CBD) Cancer –
Endocannabinoids such as anandamide AEA are important lipid ligands regulating cell proliferation, differentiation and apoptosis. Breast tumor cells express FAAH abundantly. Cell cycle arrest is responsible for apoptotic cell death. This effect is occurred by inhibition of the cyclin-dependent kinase CDK2 [ 50 , 60 ].
Cannabinoids inhibit key signaling targets in triple negative breast cancer which has worse prognosis in patients. CBD enhances the interaction between beclin1 and Vps34; it inhibits the association between beclin1 and Bcl-2 [ 63 ]. Thus, cannabinoids along with COX-2 inhibitors or other chemotherapeutic agents may represent as novel chemopreventive tools for the treatment of breast cancer. Prostate cancer is the most common malignancy among men of all races and is one of the leading causes of cancer death in this population.
JWH triggered a de novo synthesis of ceramide, which induced cell death, followed by JNK c-Jun N-terminal kinase activation and Akt inhibition [ 76 ]. Interestingly, R -methanandamide was shown to have a mitogenic effect on LNCaP cells at very low doses [ 46 , 75 ]. A recent report showed that FAAH is also over-expressed in prostate cancer cells and the inhibition of FAAH can enhance the survival of cancer patient [ 80 - 81 ]. Lung cancer has one of the highest mortality rates among cancer-suffering patients.
These results generate a rationale for further in vivo efficacy studies with this compound in preclinical cancer models. Melanoma is the mainly cause of skin cancer—related deaths worldwide.
CB1 and CB2 receptors are expressed in normal skin and skin tumors of mice and humans [ 85 ]. C57 and HaCa4 and reduces malignant tumors in nude mice [ 85 ]. WIN, or JWH induced G1 cell cycle arrest on melanoma cells, via inhibition of p-Akt and hypophosphorylation of the pRb retinoblastoma protein tumor suppressor [ 85 ].
Pancreatic cancer is one of the most aggressive and devastating human malignancies. Cannabinoid receptors on pancreatic cancer cells may affect prognosis and pain status of PDAC patients [ 86 ].
Cannabinoid administration leads to apoptosis of pancreatic tumor cells via CB2 receptor and ceramide-dependent up-regulation of p8 and ATF-4 and TRB3 stress—related genes [ 87 ]. Chondrosarcoma and osteosarcoma are the most frequent primary bone cancers [ 89 ].
Bone metastases are a frequent complication of cancer and the most frequent type of pain related to cancer. Breast cancer and prostate cancer mainly metastasize to bone which act as a fertile soil for the growth of secondary tumors [ 90 ].
The skeletal endocannabinoid system plays a significant role in regulating bone mass and bone turnover. The expression levels of CB1 and CB2 receptors were analyzed in bone cancer patient using immunohistochemistry [ 91 ].
Bone metastatic patient has severe pain so cannabinoids can attenuate pain and hyperalgesia [ 92 ]. Sativex is the combination of deltatetra-hydrocannabinol and cannabidiol, used to treat pain in cancer [ 92 ]. Effects of subcutaneously administered WIN55, on weight bearing and mechanical hyperalgesia were consistent with cannabinoid receptor mediated anti-nociception [ 93 ].
WIN55, also attenuates tumour-evoked mechanical hyperalgesia following local intraplantar administration through activation of CB1 and CB2 receptors [ 95 ]. Injection of CP55 produced anti-nociceptive properties in the tail flick test and suppressed mechanical hyperalgesia in NCTC or melanoma BF10 xenografted bone tumor model [ 96 ].
Indeed, intraplantar administration of AEA reduces mechanical hyperalgesia, URB increases AEA levels and decreases hyperalgesia in a model of calcaneous bone cancer pain [ 91 ].
However, intrathecal administration of either URB or MGL URB inhibitors failed to produce anti-nociception when tested for spontaneous flinches, limb use and weight bearing [ 97 ]. Moreover, the CB1 agonist arachidonoylchloroethylamide ACEA produces anti—nociceptive properties following intrathecal administration in this model; ACEA suppressed spontaneous flinches and increased limb use and weight bearing [ 97 ]. AM produces significantly reduced bone loss and decreased the incidence of cancer-induced bone fractures [ 94 , 98 ].
Administration of JWH and AM attenuated tumor-evoked tactile allodynia and thermal hyperalgesia by reducing NR2B-dependent activity [ 98 - 99 ]. JWH increased survival without the major side effects of current therapeutic options. Gliomas are the most important group of malignant primary brain tumors and one of the most aggressive forms of cancer, exhibit high resistance to conventional chemotherapies.
CB2 expression levels were higher in glioblastoma tissues in comparison to CB1. Selective CB2 agonists may become important targets for the treatment of glioma. Cannabinoids, inhibit tumor growth in animal models by inducing apoptosis of tumor cells and impairing tumor angiogenesis. The growth inhibitory effect of these cannabinoids is prevented by blocking ceramide synthesis, and the expression of the stress protein p8 [ - ].
The activation of this pathway was necessary for the antitumor action of cannabinoids in vivo [ ]. Glioma cells develop resistance to cannabinoid treatment due to the upregulation of Amphiregulin EGFR family ligand and the growth factor midkine Mdk [ - ].
Amphiregulin expression was associated with increased ERK activation and Mdk mediated its protective effect through ALK which interferes with autophagic cell death [ ]. The silencing of amphiregulin and Mdk or ALK pharmacological inhibition can overcome drug resistance of glioma to cannabinoids antitumoral action. Furthermore, to improve the efficacy of cannabinoids action, microencapsulation methods were used which facilitates a sustained release of the two cannabinoids for several days [ ].
In contrast, cannabinoids decreased cell viability as assessed by metabolic activity. The persistent expression of mammalian homolog of Atg8 with microtubule-associated protein-1 light chain-3 II LC3 II and p62, as well as the lack of protection from chloroquine, indicates that lysosomal degradation is not involved in this cytoplasmic vacuolation process, distinguishing from classical autophagy [ ].
Paraptosis-like cell death-a third type of a programmed cell death occurred in response to cannabinoids [ ]. Oral cancer is mainly occurs in the mouth including lips, tongue and throat. Smoking, tobacco chewing and alcohol consumption increases the incidence of oral cancer. Radiation therapy and surgery is the common treatment for oral cancer. Marijuana smoking increases the incidence of head and neck cancer in young people but its constituent, cannabinoids have anti-tumor properties.
Thyroid carcinoma is the most aggressive form which occurs in thyroid gland. IL gene transfer in to anaplastic thyroid carcinoma cell line ARO has anti-tumorigenic effect [ ]. This effect was observed due to the activation of cannabinoid receptor. Migration and invasion are characteristic features of cancer cells.
Carcinoma cells that are invasive have higher migratory potential which helps them to disseminate into the surrounding tissues and spread to other organs, ultimately leading to metastasis [ ]. Angiogenesis, which involves growth of new vasculature has been shown to be closely related to cancer metastasis. Developing novel anti-invasive and anti-angiogenic targets would be more effective in inhibiting metastasis at earlier stage [ ].
In lung cancer, CBD inhibits invasion of A cells both in vitro and in vivo that was accompanied by up-regulation of tissue inhibitor of matrix metalloproteinase-1 TIMP-1 and decreased expression of plasminogen activator inhibitor-1 PAI-1 [ - ]. In skin cancer, treatment of WIN, or JWH caused impairment of tumor vascularization and decreased expression of proangiogenic factors such as VEGF, placental growth factor, and angiopoietin-2 [ 85 ]. In glioma, [ ], one study reveals that CBD also inhibits angiogenesis by modulating MMP-2 pathway and Id-1 gene expression in glioblastoma cells [ - ].
CBD inhibits cell proliferation and invasion of 4T1 cells mammary metastatic cell line and reduces primary tumor volume as well as lung metastasis in 4T1-xenografted orthotopic model of nude mice [ - ]. This anti-metastatic effect was mediated by downregulation of Id-1 a basic helix-loop-helix transcription factor inhibitor , ERK and also by inhibiting the ROS pathway.
Furthermore, CBD reduced the number of metastatic foci in 4T1- tail vein injected syngenic model. Cancer stem cells CSC are part of the tumor cell population. Though they might be very less in number, they have the ability to self renew and replicate to produce enormous cancer cell types. CSCs have been shown to be drug resistant with higher invasive and metastatic potential [ ]. Studies show that cannabinoid receptors are involved in differentiation of neural progenitors from ectoderm and hematopoietic progenitors from mesoderm.
CB1 and CB2 receptor activation modulate proliferation and differentiation of daughter progenitors. It involved partial regulation by cannabinoid receptors leading to oxidative stress, necrosis coupled with apoptosis. These open further investigation on the function of cannabinoids and the link between stem cell and tumor progression. Increased ROS production has been associated with triggering of apoptosis [ ]. Id-1, an inhibitor of basic helix-loop-helix transcription factors, has recently been shown to be a key regulator of the metastatic potential of breast and additional cancers [ - ].
The combination of cannabinoids and gemcitabine, a nucleoside analogue used in cancer chemotherapy, synergistically inhibit pancreatic adenocarcinoma cell growth by a ROS-mediated autophagy induction without affecting normal fibroblasts [ ].
Cannabidiol CBD -induced endoplasmic reticulum stress mediated cell death of MDA-MB breast cancer cells, with the coexistence of autophagy and apoptosis [ 63 ]. In primary lymphocytes, treatment with CBD induced caspase 8 induced apoptosis which was mediated by oxidative stress. Similar result has been reported in glioma cells where CBD causes oxidative stress and higher enzymatic activities of glutathione reductase and glutathione peroxidase.
KM induced mitochondrial depolarization, cleaved caspase 3, significant cytoskeletal contractions, and redistribution of the Golgi-endoplasmic reticulum structures in U87MG human GBM cells [ ]. Cancer is a type of inflammatory disease, where immune cells infiltrate into the tumor site and secrete factors which enhance the prospects of proliferation, angiogenesis and metastasis [ ].
Hence, it is important to identify anti-cancer agents that target the immune related cancer environment. In glioma, WIN, caused accumulation of ceramide which is essential for cell death and it also had anti-inflammatory effects [ ].
Cannabinoids exert a direct anti-proliferative effect on tumors of different origin. They have been shown to be anti-migratory and anti-invasive and inhibit MMPs which in turn degrade the extra-cellular matrix ECM , thus affecting metastasis of cancer to the distant organs.
Also, cannabinoids modulate other major processes in our body like energy metabolism, inflammation, etc. These data are derived not only from cell culture systems but also from more complex and clinically relevant animal models. Before cannabinoids could be used in clinical trials, there is need to explore more knowledge on several issues such as anti-tumorigenic and anti-metastatic mechanisms as well as which type of cancer patient populations would be more responsive for cannabinoid based therapies.
Data presented in this review suggest that cannabinoids derived from different sources regulate differently signaling pathways, modulate different tumor cell types and host physiological system. It is important to understand which of the cannabinoid receptors are expressed and activated in different tumors as each receptor follows a different signaling mechanism. Furthermore, endocannabinoids- AEA and 2-AG are broken down into secondary metabolites like prostaglandin PGE 2 and epoxyeicosatetraenoic acid EE which enhance tumor growth and metastasis in diverse cancer types.
Understanding the exact signaling by which cannabinoids function will eventually lead to targeted clinical approach. Also, the difference in cellular response to cannabinoids in different cancer types might be due to the effect of the tumor environment which involves inflammatory cells, fibroblasts, endothelial cells, macrophages, etc. Thus, there is a need for an integrative understanding of the role of cannabinoids with respect to the tumor and its microenvironment. The diversity of affecting multiple signaling pathways might pave way for developing cannabinoids that selectively obstruct a particular pathway, thus opening avenues for specific targeted treatments.
Moreover, cannabinoids are more specific to cancer cells than normal cells. The administration of single cannabinoids might produce limited relief compared to the administration of crude extract of plant containing multiple cannabinoids, terpenes and flavanoids.
Thus, combination of cannabinoids with other chemotherapeutic drugs might provide a potent clinical outcome, reduce toxicity, increase specificity and overcome drug resistance complications. Additional findings in in vitro and in vivo models are needed to support studies at preclinical setting. The authors disclose no competing interests. National Center for Biotechnology Information , U. Journal List Oncotarget v.
Published online Jul Author information Article notes Copyright and License information Disclaimer. Received May 19; Accepted Jul This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
This article has been cited by other articles in PMC. Abstract The pharmacological importance of cannabinoids has been in study for several years. Cannabinoid receptors, cannabinoid agonists, cancer, signaling. Cannabinoid and its receptor Cannabinoids can be classified into three groups based on their source of production; endogenous cannabinoids endocannabinoids , phytocannabinoids and synthetic cannabinoids Fig.
Table I Cannabinoid's structure and its role in different physiological processes. Docosatetraenyl ethanolamide CB1 agonist neuromodulatory and immunomodulatory [ ]. Oleamide CB1 agonist neuromodulatory and immunomodulatory [ ].
Open in a separate window. Cannabinoids and their classification This figure illustrates how cannabinoids are divided into three main categories according to their availability in nature.
Endogenous cannabinoids Endogenous cannabinoids which are produced in our body include lipid molecules containing long-chain polyunsaturated fatty acids, amides, esters and ethers that bind to CB1 or CB2 receptors. Phytocannabinoids Phytocannabinoids are only known to occur naturally in significant quantity in the cannabis plant, and are concentrated in a viscous resin that is produced in glandular structures known as trichomes.
Synthetic cannabinoids Synthetic cannabinoids have been extensively used as a pharmacological agent, both in vitro and in vivo , to obtain more detailed insight of cannabinoid action, in order to evaluate their potential clinical use. Cannabinoid mediated signaling in cancer cells Cannabinoids activate CB1 or CB2 receptor which in turn modulates diverse signaling targets. Table II Role of cannabinoid in different cancers and its associated signaling. Cannabinoids Anti-cancer effect and its mechanism of action Anandamide 1 Breast cancer: Suppression of nerve growth factor Trk receptors and prolactin receptors Prostate cancer: Attenuates mechanical hyperalgesia HU 1 Prostate cancer: MMPs pathway 3 Skin cancer: Mitogenic at low doses 4 Glioma: Role of cannabinoids in regulation of cancer growth One of the important aspects of an effective anti-tumor drug is its ability to inhibit proliferation of cancer cells.
Cannabinoids and breast cancer Breast cancer is one of the most common human malignancies and the second leading cause of cancer-related deaths in women, and its incidence in the developing world is on the rise [ 40 - 41 ]. Cannabinoids and prostate cancer Prostate cancer is the most common malignancy among men of all races and is one of the leading causes of cancer death in this population.
Cannabinoids and lung cancer Lung cancer has one of the highest mortality rates among cancer-suffering patients. Cannabinoids and skin cancer Melanoma is the mainly cause of skin cancer—related deaths worldwide. Cannabinoids and pancreatic cancer Pancreatic cancer is one of the most aggressive and devastating human malignancies. Cannabinoids and bone cancer Chondrosarcoma and osteosarcoma are the most frequent primary bone cancers [ 89 ].
Cannabinoids and glioma Gliomas are the most important group of malignant primary brain tumors and one of the most aggressive forms of cancer, exhibit high resistance to conventional chemotherapies.
National Academies Press US ; Changes in cannabis potency over the last 2 decades Cannabis smoking and lung cancer risk: An epidemiologic review of marijuana and cancer: Cancer Epidemiol Biomarkers Prev. American Society of Clinical Oncology clinical practice guideline update. Dronabinol versus megestrol acetate versus combination therapy for cancer-associated anorexia: Friedman D, Devinsky O.
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Lung cancer patient SHRUNK tumour ‘using cannabidiol CBD oil’
Other common cannabinoids are cannabidiol (CBD), Cannabigerol . 3)Lung cancer: up-regulation of TIMP-1 Cox-2 and PPAR-γ regulation. CBD may therefore represent a more useful therapeutic agent. To address this gap in our knowledge, scientists used lung cancer cell lines and cells derived. this action. In the lung cancer cell lines A, H, and H, cannabidiol (CBD ; –3 M) elicited concentration-dependent ICAM-1 up-regulation com-.