Cannabinoids and cancer: potential for colorectal cancer therapy

2005 ◽  
Vol 33 (4) ◽  
pp. 712-714 ◽  
Author(s):  
H.A. Patsos ◽  
D.J. Hicks ◽  
A. Greenhough ◽  
A.C. Williams ◽  
C. Paraskeva

Despite extensive research into the biology of CRC (colorectal cancer), and recent advances in surgical techniques and chemotherapy, CRC continues to be a major cause of death throughout the world. Therefore it is important to develop novel chemopreventive/chemotherapeutic agents for CRC. Cannabinoids are a class of compounds that are currently used in the treatment of chemotherapy-induced nausea and vomiting, and in the stimulation of appetite. However, there is accumulating evidence that they could also be useful for the inhibition of tumour cell growth by modulating key survival signalling pathways. The chemotherapeutic potential for plant-derived and endogenous cannabinoids in CRC therapy is reviewed.

Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1952
Author(s):  
Crescenzo D’Alterio ◽  
Antonella Zannetti ◽  
Anna Maria Trotta ◽  
Caterina Ieranò ◽  
Maria Napolitano ◽  
...  

The chemokine receptor CXCR4 is overexpressed and functional in colorectal cancer. To investigate the role of CXCR4 antagonism in potentiating colon cancer standard therapy, the new peptide CXCR4 antagonist Peptide R (Pep R) was employed. Human colon cancer HCT116 xenograft-bearing mice were treated with chemotherapeutic agents (CT) 5-Fluorouracil (5FU) and oxaliplatin (OX) or 5FU and radio chemotherapy (RT-CT) in the presence of Pep R. After two weeks, CT plus Pep R reduced by 4-fold the relative tumor volume (RTV) as compared to 2- and 1.6-fold reductions induced, respectively, by CT and Pep R. In vitro Pep R addition to CT/RT-CT impaired HCT116 cell growth and further reduced HCT116 and HT29 clonal capability. Thus, the hypothesis that Pep R could target the epithelial mesenchyme transition (EMT) process was evaluated. While CT decreased ECAD and increased ZEB-1 and CD90 expression, the addition of Pep R restored the pretreatment expression. In HCT116 and HT29 cells, CT/RT-CT induced a population of CD133+CXCR4+ cells, supposedly a stem-resistant cancer cell population, while Pep R reduced it. Taken together, the results showed that targeting CXCR4 ameliorates the effect of treatment in colon cancer through inhibition of cell growth and reversal of EMT treatment-induced markers, supporting further clinical studies.


2019 ◽  
Vol 10 (6) ◽  
pp. 3748-3757 ◽  
Author(s):  
Lihua Wang ◽  
Zheng Zhu ◽  
Lei Han ◽  
Liqian Zhao ◽  
Jialei Weng ◽  
...  

HCC is a common cancer type in the world. Here, we found WZ35, a novel derivative of curcumin, could notably suppress HCC cell growthviainhibiting YAP controlled autophagy, highlighting the potent anti-tumor activity of WZ35 in liver cancer therapy.


2020 ◽  
Vol 54 (3) ◽  
pp. 272-277
Author(s):  
Martina Rebersek

AbstractBackgroundColorectal cancer (CRC) is one of the most common types of cancer in the world. Metastatic disease is still incurable in most of these patients, but the survival rate has improved by treatment with novel systemic chemotherapy and targeted therapy in combination with surgery. New knowledge of its complex heterogeneity in terms of genetics, epigenetics, transcriptomics and microenvironment, including prognostic and clinical characteristics, led to its classification into various molecular subtypes of metastatic CRC, called consensus molecular subtypes (CMS). The CMS classification thus enables the medical oncologists to adjust the treatment from case to case. They can determine which type of systemic chemotherapy or targeted therapy is best suited to a specific patient, what dosages are needed and in what order.ConclusionsCMS in metastatic CRC are the new tool to include the knowledge of molecular factors, tumour stroma and signalling pathways for personalized, patient-orientated systemic treatment in precision medicine.


2009 ◽  
Vol 37 (4) ◽  
pp. 910-913 ◽  
Author(s):  
John H. Bannon ◽  
Margaret M. Mc Gee

The role of aneuploidy in tumorigenesis remains poorly understood, although the two have been known to be linked for more than 100 years. Recent studies indicate that aneuploidy can promote tumour cell growth and cell death and that the cellular outcome is dependent on the extent of aneuploidy induced. The mitotic checkpoint plays a pivotal role in the maintenance of genome stability and has been the focus of work investigating the distinct outcomes of aneuploidy. In the present article, we review the molecular mechanisms involved and discuss the potential of the mitotic checkpoint as a therapeutic target in cancer therapy.


2018 ◽  
Vol 22 (5) ◽  
pp. 17-24 ◽  
Author(s):  
E. V. Burnasheva ◽  
Y. V. Shatokhin ◽  
I. V. Snezhko ◽  
A. A. Matsuga

Кidney injury is a frequent and significant complication of cancer and cancer therapy. The kidneys are susceptible to injury from malignant infiltration, damage by metabolites of malignant cells, glomerular  injury, nephrotoxic drugs including chemotherapeutic agents. Also  bone marrow transplantation complications, infections with immune  suppression (including septicemia), tumor lysis syndrome should be  taken into account. Chemotherapeutic agents are a common cause  of acute kidney injury but can potentially lead to chronic kidney  disease development in cancer patients. This article summarizes risk  factors of acute kidney injury in cancer patients. Risk factors are  divided into two groups. The systemic are decrease of total  circulating blood volume, infiltration of kidney tissue by tumor cells,  dysproteinemia, electrolyte disturbances. The local (renal) risk  factors are microcirculation disturbances, drugs biotransformation  with formation of reactive oxygen intermediates, high concentration of nephrotoxic agents in proximal tubules and its  sensitivity to ischemia. Drug-related risk factors include: drugs  combination with cytotoxic effect high doses long term use necessity, direct cytotoxic effect of not only chemotherapeutic agents but also its metabolites, mean solubility forming intratubular  precipitates. Early diagnosis, timely prevention and treatment of  these complications provide significantly improve nononcologic results of treatment.


Author(s):  
Ricardo Salomao Aboud ◽  
Jose Daniel Diaz ◽  
Alfredo Mendez ◽  
Leonard John Kalfayan ◽  
Lance Nigel Portman ◽  
...  

2020 ◽  
Vol 27 (13) ◽  
pp. 2118-2132 ◽  
Author(s):  
Aysegul Hanikoglu ◽  
Hakan Ozben ◽  
Ferhat Hanikoglu ◽  
Tomris Ozben

: Elevated Reactive Oxygen Species (ROS) generated by the conventional cancer therapies and the endogenous production of ROS have been observed in various types of cancers. In contrast to the harmful effects of oxidative stress in different pathologies other than cancer, ROS can speed anti-tumorigenic signaling and cause apoptosis of tumor cells via oxidative stress as demonstrated in several studies. The primary actions of antioxidants in cells are to provide a redox balance between reduction-oxidation reactions. Antioxidants in tumor cells can scavenge excess ROS, causing resistance to ROS induced apoptosis. Various chemotherapeutic drugs, in their clinical use, have evoked drug resistance and serious side effects. Consequently, drugs having single-targets are not able to provide an effective cancer therapy. Recently, developed hybrid anticancer drugs promise great therapeutic advantages due to their capacity to overcome the limitations encountered with conventional chemotherapeutic agents. Hybrid compounds have advantages in comparison to the single cancer drugs which have usually low solubility, adverse side effects, and drug resistance. This review addresses two important treatments strategies in cancer therapy: oxidative stress induced apoptosis and hybrid anticancer drugs.


2012 ◽  
Vol 24 (10) ◽  
pp. 1940-1949 ◽  
Author(s):  
Yun Hee Kang ◽  
Na Young Ji ◽  
Seung Ro Han ◽  
Chung Il Lee ◽  
Jae Wha Kim ◽  
...  

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