scholarly journals Development of NOSH-NSAIDs: a new class of anti-inflammatory pharmaceuticals for the treatment of cancer

2017 ◽  
Vol 39 (4) ◽  
pp. 24-29
Author(s):  
Khosrow Kashfi

Non-steroidal anti-inflammatory drugs (NSAIDs) have anti-cancer (chemopreventive) properties; however, side effects preclude their long-term use. NOSH-NSAIDs, designed as safer alternatives, are novel hybrid chimaeras that release nitric oxide (NO) and hydrogen sulfide (H2S). NOSH-NSAIDs are gastrointestinally safe yet retain all the pharmacological properties of their native NSAID. NOSHNSAIDs are orders of magnitude more potent than their conventional counterparts in inhibiting the growth of various human cancer cell lines of different tissue origins, adenomatous, epithelial and lymphocytic. This growth inhibition is a result of a reduction in cell proliferation and cell cycle arrest, leading to increased apoptosis. In xenograft mouse models of cancer, NOSH-aspirin was better than normal aspirin as a chemopreventive agent; it dose-dependently inhibited tumour growth and tumour mass. NOSH-naproxen was significantly more efficacious than normal naproxen in reducing the growth of established tumours.

Molecules ◽  
2022 ◽  
Vol 27 (1) ◽  
pp. 284
Author(s):  
Abdelhakim Bouyahya ◽  
Aicha El Allam ◽  
Ikrame Zeouk ◽  
Douae Taha ◽  
Gokhan Zengin ◽  
...  

Grifolin is a volatile compound contained in essential oils of several medicinal plants. Several studies show that this substance has been the subject of numerous pharmacological investigations, which have yielded interesting results. Grifolin demonstrated beneficial effects for health via its multiple pharmacological activities. It has anti-microbial properties against bacteria, fungi, and parasites. In addition, grifolin exhibited remarkable anti-cancer effects on different human cancer cells. The anticancer action of this molecule is related to its ability to act at cellular and molecular levels on different checkpoints controlling the signaling pathways of human cancer cell lines. Grifolin can induce apoptosis, cell cycle arrest, autophagy, and senescence in these cells. Despite its major pharmacological properties, grifolin has only been investigated in vitro and in vivo. Therefore, further investigations concerning pharmacodynamic and pharmacokinetic tests are required for any possible pharmaceutical application of this substance. Moreover, toxicological tests and other investigations involving humans as a study model are required to validate the safety and clinical applications of grifolin.


2007 ◽  
Vol 24 ◽  
pp. 88-95 ◽  
Author(s):  
T. OHKUSA ◽  
T. TERAI ◽  
S. ABE ◽  
O. KOBAYASHI ◽  
K. BEPPU ◽  
...  

2021 ◽  
Vol 23 (3) ◽  
Author(s):  
V. V. Buheruk ◽  
O. B. Voloshyna ◽  
L. I. Kovalchuk ◽  
I. V. Balashova ◽  
O. V. Naidionova

The aim of this review is to analyze and summarize the existing evidence regarding the possibilities of using acetylsalicylic acid (ASA) and other non-steroidal anti-inflammatory drugs (NSAIDs) to reduce cancer risk. Conclusions. Chronic inflammation facilitates the onset and progress of tumour growth. Anti-cancer properties of acetylsalicylic acid and other non-steroidal anti-inflammatory drugs are mediated via cyclooxygenase COX-dependent mechanisms, as well as other tumorigenic pathways. Current systematic review addresses potential role of ASA and other NSAIDs in reduction of cancer risk for the following localizations: head and neck, lungs, gastrointestinal tract, breast, ovaries, prostate, and skin. The role of ASA in primary prevention of colorectal cancer in specific populations is presented in 2016 U. S. Preventive Services Task Force guidelines. Studies indicate heterogeneous protective potential of ASA against different cancer types, depending on studied population, duration of intake and dose. Influence of non-aspirin NSAIDs on cancer morbidity and mortality is more controversial.


2021 ◽  
Author(s):  
Long Jiang ◽  
Katrine Ingelshed ◽  
Yunbing Shen ◽  
Sanjaykumar V. Boddul ◽  
Vaishnavi Srinivasan Iyer ◽  
...  

CRISPR/Cas9 can be used to inactivate or modify genes by inducing double-stranded DNA breaks1–3. As a protective cellular response, DNA breaks result in p53-mediated cell cycle arrest and activation of cell death programs4,5. Inactivating p53 mutations are the most commonly found genetic alterations in cancer, highlighting the important role of the gene6–8. Here, we show that cells deficient in p53, as well as in genes of a core CRISPR-p53 tumor suppressor interactome, are enriched in a cell population when CRISPR is applied. Such enrichment could pose a challenge for clinical CRISPR use. Importantly, we identify that transient p53 inhibition suppresses the enrichment of cells with these mutations. Furthermore, in a data set of >800 human cancer cell lines, we identify parameters influencing the enrichment of p53 mutated cells, including strong baseline CDKN1A expression as a predictor for an active CRISPR-p53 axis. Taken together, our data identify strategies enabling safe CRISPR use.


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