scholarly journals Do NSAIDs Prevent Colorectal Cancer?

2000 ◽  
Vol 14 (4) ◽  
pp. 299-307 ◽  
Author(s):  
Nadir Arber
Keyword(s):  
Colorectal Cancer ◽  
Animal Studies ◽  
Molecular Mechanisms ◽  
Drug Induced ◽  
Cycle Arrest ◽  
Preventive Activity ◽  
Frequency Of Use ◽  
Familial Adenomatosis Coli ◽  
Inflammatory Drugs ◽  
Induction Of Apoptosis

There is increasing evidence to suggest that acetylsalicylic acid (ASA) and other nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the risk of colorectal cancer. This observation is supported by animal studies that show fewer tumours per animal and fewer animals with tumours after administration of several different NSAIDs. Studies in humans consistently support this hypothesis. Intervention data from familial adenomatosis coli establish that the process of human colonic adenoma polyp formation is affected. Supportive evidence comes from 21 of 23 human studies -- both case-control and cohort. The reduced risk has been found in men and women, for cancers of the colon and the rectum and for the use of both ASA and the other NSAIDs. Earlier detection of lesions as a result of drug-induced bleeding does not seem to account for these findings. The molecular mechanisms responsible for the chemopreventive action of this class of drugs is not completely established. Protection may affect several pathways, including cell cycle arrest and induction of apoptosis.  Because of the consistency of epidemiological, clinical and experimental data, there is no need for further placebo trials. At the same time, there is a need to establish the dose, duration and frequency of use required for cancer-preventive activity.

scholarly journals Resistance to glucocorticoid-induced apoptosis in lymphoblastic leukemia

2003 ◽  
Vol 178 (1) ◽  
pp. 19-27 ◽  
Author(s):  
R Kofler ◽  
S Schmidt ◽  
A Kofler ◽  
MJ Ausserlechner
Keyword(s):  
Molecular Mechanisms ◽  
Lymphoblastic Leukemia ◽  
Resistance Mechanisms ◽  
Lymphoid Malignancies ◽  
Cycle Arrest ◽  
Major Significance ◽  
Induction Of Apoptosis ◽  
Review Reports ◽  
Induced Apoptosis

Glucocorticoid (GC) resistance is a phenomenon of major significance in a number of clinical situations, including the therapy of lymphoid malignancies. Resistance may concern all, or just selected, GC effects, it may be absolute or just reflect a state of reduced sensitivity and, clinically relevant, be reversible or irreversible. Numerous molecular mechanisms can be envisaged acting either 'upstream' in the GC-triggered signaling pathway, i.e. at the level of the GC receptor (GR), or 'downstream' at the level of the GC-regulated genes responsible for individual GC effects. In lymphoid malignancies, GCs have anti-leukemic effects through the induction of apoptosis and/or cell cycle arrest. In this condition evidence for only a small number of mechanisms for GC resistance has been provided, mostly at the level of the GR. Herein, we review reports and hypotheses regarding 'upstream' and 'downstream' mechanisms for GC resistance in lymphoblastic leukemia and present an in vitro GC resistance model that might allow identification of resistance mechanisms.

scholarly journals In Vivo and In Vitro Effects of Tracheloside on Colorectal Cancer Cell Proliferation and Metastasis

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 513
Author(s):  
Min-Kyoung Shin ◽  
Yong-Deok Jeon ◽  
Seung-Heon Hong ◽  
Sa-Haeng Kang ◽  
Ji-Ye Kee ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Oxidant Stress ◽  
Mesenchymal Transition ◽  
Cycle Arrest

Recent research suggests a relationship between cancer progression and oxidative mechanisms. Among the phenolic compounds such as tracheloside (TCS) are a major bioactive compound that can combat oxidant stress-related chronic diseases and that also displays anti-tumor activity. Although TCS can inhibit mammalian carcinoma, its effects on colorectal cancer (CRC) have not been clarified. The purpose of this study was to investigate the effects of TCS on the proliferation of CRC cells, the metastasis of CT26 cells, and the molecular mechanisms related to TCS in vitro and in vivo. A cell viability assay showed that TCS inhibited the proliferation of CRC cells. TCS-treated CT26 cells were associated with the upregulation of p16 as well as the downregulation of cyclin D1 and CDK4 in cell cycle arrest. In addition, TCS induced apoptosis of CT26 cells through mitochondria-mediated apoptosis and regulation of the Bcl-2 family. Expression of epithelial–mesenchymal transition (EMT) markers was regulated by TCS treatment in CT26 cells. TCS significantly inhibited the lung metastasis of CT26 cells in a mouse model. These results suggest that TCS, by inducing cell cycle arrest and apoptosis through its anti-oxidant properties, is a novel therapeutic agent that inhibits metastatic phenotypes of murine CRC cells.

scholarly journals Hsa-miR-3658 down-regulates OCT4 gene expression followed by suppressing SW480 cell proliferation and migration

2020 ◽  
Vol 477 (12) ◽  
pp. 2281-2293
Author(s):  
Fahimeh Hosseini ◽  
Bahram M. Soltani ◽  
Hossein Baharvand ◽  
Saman Hosseinkhani
Keyword(s):  
Gene Expression ◽  
Colorectal Cancer ◽  
Molecular Mechanisms ◽  
Direct Interaction ◽  
Scratch Test ◽  
Sw480 Cell ◽  
Luciferase Assay ◽  
Cycle Arrest ◽  
Bona Fide ◽  
And Migration

The pluripotency factor, OCT4 gene is a stemness marker that is involved in the tumorigenicity of different cancer types and knowing about molecular mechanisms of its regulation is crucially important. To date, a few microRNAs (miRNAs) are known to be regulators of OCT4 gene expression. Looking for the novel miRNAs which are capable of regulating OCT4 gene expression, our bioinformatics analysis introduced hsa-miR-3658 (miR-3658) as a bona fide candidate. Then, RT-qPCR results indicated that miR-3658 expression is decreased in colorectal cancer (CRC) tumor tissues, compared with normal pairs. Furthermore, RT-qPCR and western blot analysis showed that the OCT4 gene has been down-regulated following the miR-3658 overexpression. Consistently, dual-luciferase assay supported the direct interaction of miR-3658 with the 3′-UTR sequence of OCT4 gene. Unlike in HCT116 cells, overexpression of miR-3658 in SW480 cells brought about growth inhibition, cell cycle arrest and reduced cell migration, detected by flow cytometry, and scratch test assay. Overall, these findings demonstrated that miR-3658 as a tumor suppressor miRNA exerts its effect against OCT4 gene expression, and it has the potential of being used as a prognostic marker and therapeutic target against colorectal cancer.

scholarly journals Antineoplastic mechanisms of niclosamide-loaded nanoparticles in human colorectal cancer cells

2017 ◽  
Vol 63 (2) ◽  
pp. 132-138 ◽  
Author(s):  
A.S. Zhirnik ◽  
Y.P. Semochkina ◽  
E.Yu. Moskaleva ◽  
N.I. Krylov ◽  
I.A. Tubasheva ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Lung Fibroblasts ◽  
Human Colorectal Cancer ◽  
Human Embryonic Lung ◽  
Polymeric Form ◽  
Mitochondrial Superoxide ◽  
Cycle Arrest ◽  
Human Colorectal Cancer Cell

Using poly(lactic-co-glycolic) acid we developed a polymeric form of niclosamide (PFN) and investigated molecular mechanisms underlying its antitumor activity against human colorectal cancer cell lines (SW837, Caco-2, COLO 320 HSR). PFN was shown to be more cytotoxic against cancer cells and less cytotoxic against normal cells (human embryonic lung fibroblasts) as compared to niclosamide. Both niclosamide and its polymeric form caused mitochondrial damage (evaluated as a decrease in rhodamine 123 accumulation) and increased the levels of reactive oxygen species, particularly mitochondrial superoxide, resulting in the oxidative damage to biomolecules. Furthermore, niclosamide and PFN induced G0/G1 cell cycle arrest.

scholarly journals The Impact of Probiotics on Intestinal Mucositis during Chemotherapy for Colorectal Cancer. A Comprehensive Review of Animal Studies

2021 ◽  
Vol 22 (17) ◽  
pp. 9347
Author(s):  
Povilas Miknevicius ◽  
Ruta Zulpaite ◽  
Bettina Leber ◽  
Kestutis Strupas ◽  
Philipp Stiegler ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Side Effects ◽  
Animal Studies ◽  
Combined Treatment ◽  
Experimental Studies ◽  
Current Treatment ◽  
Treatment Modalities ◽  
Drug Induced ◽  
Intestinal Mucositis ◽  
The Impact

Colorectal cancer (CRC) is the second most commonly diagnosed cancer in females (incidence 16.4/10000) and the third in males (incidence 23.4/10000) worldwide. Surgery, chemotherapy (CTx), radiation therapy (RTx), or a combined treatment of those are the current treatment modalities for primary CRC. Chemotherapeutic drug-induced gastrointestinal (GIT) toxicity mainly presents as mucositis and diarrhea. Preclinical studies revealed that probiotic supplementation helps prevent CTx-induced side effects by reducing oxidative stress and proinflammatory cytokine production and promoting crypt cell proliferation. Moreover, probiotics showed significant results in preventing the loss of body weight (BW) and reducing diarrhea. However, further clinical studies are needed to elucidate the exact doses and most promising combination of strains to reduce or prevent chemotherapy-induced side effects. The aim of this review is to overview currently available literature on the impact of probiotics on CTx-induced side effects in animal studies concerning CRC treatment and discuss the potential mechanisms based on experimental studies’ outcomes.

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