Abstract:Background:The prominent hallmark of malignancies is the metastatic spread of cancer cells. Recent studies have reported that the nature of invasive cells could be changed after this phenomenon, causing chemotherapy resistance. It has been demonstrated that the up-regulated expression of matrix metalloproteinase (MMP) 2/MMP-9, as a metastasis biomarker, can fortify the metastatic potential of leukemia. Furthermore, investigations have confirmed the inhibitory effect of cannabinoid and endocannabinoid on the pr… Show more
“… 29 On the contrary, cannabinoid agonists induced apoptosis of PCa cells and reduced the size of tumors. 12 , 13 Additionally, several in vivo and in vitro studies revealed the crucial role of cannabinoid receptors in the anti‐proliferation of BCa cells. 27 , 30 …”
Section: Discussionmentioning
confidence: 99%
“…Several functional studies elaborated that cannabinoids appeared to inhibit cell proliferation, migration, and angiogenesis in urological cancer cells. 11 , 12 , 13 …”
Background
Legislation of cannabis use has been approved in many European and North American countries. Its impact on urological cancers is unclear. This study was conducted to explore the association between cannabis use and the risk of urological cancers.
Methods
We identified 151,945 individuals with information on cannabis use in the UK Biobank from 2006 to 2010. Crude and age‐standardized incidence ratios of different urological cancers were evaluated in the entire cohort and subgroups. Cox regression was performed for survival analysis.
Results
Previous use of cannabis was a significant protective factor for renal cell carcinoma (HR = 0.61, 95%CI:0.40–0.93,
p
= 0.021) and prostate cancer (HR = 0.82, 95%CI:0.73–0.93,
p
= 0.002) in multivariable analysis. The association between previous cannabis use and both renal cell carcinoma and bladder cancer was only observed in females (HR
RCC
= 0.42, 95%CI:0.19–0.94,
p
= 0.034; HR
BCa
= 0.43, 95%CI:0.21–0.86,
p
= 0.018) but not in men. There was no significant association between cannabis use and testicular cancer incidence. Mendelian randomization demonstrated a potential causal effect of cannabis use on a lower incidence of renal cell carcinoma.
Conclusions
Previous use of cannabis was associated with a lower risk of bladder cancer, renal cell carcinoma, and prostate cancer. The inverse association between cannabis and both renal cell carcinoma and bladder cancer was only found in females but not in males.
“… 29 On the contrary, cannabinoid agonists induced apoptosis of PCa cells and reduced the size of tumors. 12 , 13 Additionally, several in vivo and in vitro studies revealed the crucial role of cannabinoid receptors in the anti‐proliferation of BCa cells. 27 , 30 …”
Section: Discussionmentioning
confidence: 99%
“…Several functional studies elaborated that cannabinoids appeared to inhibit cell proliferation, migration, and angiogenesis in urological cancer cells. 11 , 12 , 13 …”
Background
Legislation of cannabis use has been approved in many European and North American countries. Its impact on urological cancers is unclear. This study was conducted to explore the association between cannabis use and the risk of urological cancers.
Methods
We identified 151,945 individuals with information on cannabis use in the UK Biobank from 2006 to 2010. Crude and age‐standardized incidence ratios of different urological cancers were evaluated in the entire cohort and subgroups. Cox regression was performed for survival analysis.
Results
Previous use of cannabis was a significant protective factor for renal cell carcinoma (HR = 0.61, 95%CI:0.40–0.93,
p
= 0.021) and prostate cancer (HR = 0.82, 95%CI:0.73–0.93,
p
= 0.002) in multivariable analysis. The association between previous cannabis use and both renal cell carcinoma and bladder cancer was only observed in females (HR
RCC
= 0.42, 95%CI:0.19–0.94,
p
= 0.034; HR
BCa
= 0.43, 95%CI:0.21–0.86,
p
= 0.018) but not in men. There was no significant association between cannabis use and testicular cancer incidence. Mendelian randomization demonstrated a potential causal effect of cannabis use on a lower incidence of renal cell carcinoma.
Conclusions
Previous use of cannabis was associated with a lower risk of bladder cancer, renal cell carcinoma, and prostate cancer. The inverse association between cannabis and both renal cell carcinoma and bladder cancer was only found in females but not in males.
“…In our experiments, we obtain a reduction in both TMBS4X gene and MMP-2 protein expression levels. While in the literature the direct effect of cannabinoids in reducing the expression of MMP-2, also attenuating invasion in leukemic cells [ 54 ], is well-documented, there are no data regarding the interaction between the TMBS4X gene and CB2 receptors. So, it could be interesting to investigate the reasons behind the reduction in gene expression after treatment with JWH-133.…”
Acute lymphoblastic leukemia type B (B-ALL) is the most common kind of pediatric leukemia, characterized by the clonal proliferation of type B lymphoid stem cells. Important progress in ALL treatments led to improvements in long-term survival; nevertheless, many adverse long-term consequences still concern the medical community. Molecular and cellular target therapies, together with immunotherapy, are promising strategies to overcome these concerns. Cannabinoids, enzymes involved in their metabolism, and cannabinoid receptors type 1 (CB1) and type 2 (CB2) constitute the endocannabinoid system, involved in inflammation, immune response, and cancer. CB2 receptor stimulation exerts anti-proliferative and anti-invasive effects in many tumors. In this study, we evaluated the effects of CB2 stimulation on B-ALL cell lines, SUP-B15, by RNA sequencing, Western blotting, and ELISA. We observe a lower expression of CB2 in SUP-B15 cells compared to lymphocytes from healthy subjects, hypothesizing its involvement in B-ALL pathogenesis. CB2 stimulation reduces the expression of CD9, SEC61G, TBX21, and TMSB4X genes involved in tumor growth and progression, and also negatively affects downstream intracellular pathways. Our findings suggest an antitumor role of CB2 stimulation in B-ALL, and highlight a functional correlation between CB2 receptors and specific anti-tumoral pathways, even though further investigations are needed.
“…Recently, cannabinoids have been shown to inhibit cell proliferation, migration, and angiogenesis, as well as arrest the cell cycle and induce apoptosis in prostate cancer cells [ 46 ]. Furthermore, a number of in vitro studies have reported that synthetic cannabinoids such as WIN55,212, JWH-133, and JWH-015 can reduce the size of prostate cancer cell-derived tumors [ 55 , 56 ]. Of the six papers examined, five used synthetic cannabinoids [ 33 , 46 , 50 , 51 , 52 ], while the other used natural cannabinoids [ 45 ].…”
Prostate cancer is a major cause of death among men worldwide. Recent preclinical evidence implicates cannabinoids as powerful regulators of cell growth and differentiation, as well as potential anti-cancer agents. The aim of this review was to evaluate the effect of cannabinoids on in vivo prostate cancer models. The databases searched included PubMed, Embase, Scopus, and Web of Science from inception to August 2020. Articles reporting on the effect of cannabinoids on prostate cancer were deemed eligible. We identified six studies that were all found to be based on in vivo/xenograft animal models. Results: In PC3 and DU145 xenografts, WIN55,212-2 reduced cell proliferation in a dose-dependent manner. Furthermore, in LNCaP xenografts, WIN55,212-2 reduced cell proliferation by 66–69%. PM49, which is a synthetic cannabinoid quinone, was also found to result in a significant inhibition of tumor growth of up to 90% in xenograft models of LNCaP and 40% in xenograft models of PC3 cells, respectively. All studies have reported that the treatment of prostate cancers in in vivo/xenograft models with various cannabinoids decreased the size of the tumor, the outcomes of which depended on the dose and length of treatment. Within the limitation of these identified studies, cannabinoids were shown to reduce the size of prostate cancer tumors in animal models. However, further well-designed and controlled animal studies are warranted to confirm these findings.
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