Chemopreventive action of non-steroidal anti-inflammatory drugs on the inflammatory pathways in colon cancer

Ghanghas, Preety; Jain, Shelly; Rana, Chandan; Sanyal, Sankar Nath

doi:10.1016/j.biopha.2016.01.024

Cited by 35 publications

(20 citation statements)

References 45 publications

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“…In another study, it was reported that a new H 2 S-releasing derivative of naproxen, ATB-346 [2-(6-methoxynapthalen-2-yl)-propionic acid 4-thiocarbamoyl phenyl ester] can abrogate proliferation and induce apoptosis via the negative regulation of NF-κB activation in human melanoma cells [ 184 ]. Moreover, the co-administration of three different NSAIDs (celecoxib, etoricoxib, and diclofenac) was found to significantly abrogate the development of the 1,2-dimethylhydrazine dihydrochloride-induced colorectal cancer via the suppression of the NF-κB activation cascade [ 185 ].…”

Section: Inhibitors Of Nf-κb Function and Selected Pharmacologicalmentioning

confidence: 99%

Evidence for the Involvement of the Master Transcription Factor NF-κB in Cancer Initiation and Progression

et al. 2018

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Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is responsible for the regulation of a large number of genes that are involved in important physiological processes, including survival, inflammation, and immune responses. At the same time, this transcription factor can control the expression of a plethora of genes that promote tumor cell proliferation, survival, metastasis, inflammation, invasion, and angiogenesis. The aberrant activation of this transcription factor has been observed in several types of cancer and is known to contribute to aggressive tumor growth and resistance to therapeutic treatment. Although NF-κB has been identified to be a major contributor to cancer initiation and development, there is evidence revealing its role in tumor suppression. This review briefly highlights the major mechanisms of NF-κB activation, the role of NF-κB in tumor promotion and suppression, as well as a few important pharmacological strategies that have been developed to modulate NF-κB function.

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Section: Inhibitors Of Nf-κb Function and Selected Pharmacologicalmentioning

confidence: 99%

Evidence for the Involvement of the Master Transcription Factor NF-κB in Cancer Initiation and Progression

et al. 2018

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“…This coincided with a delayed progression of premalignant lesions toward cancer. Consistent with these studies was demonstration that administration of selective inhibitors of cyclooxygenase-2 (COX-2) to rats diminishes the carcinogen-induced inflammatory NF-kB signaling pathways and retards development of colonic tumors [ 68 ]. Contrasting with these latter two studies, administration of the select COX-2 inhibitor celecoxib to a mouse model of Helicobacter-associated precancerous lesions tempered the immune inhibitory effects of PGE 2 on expression of the Th1 cytokine IFN-γ and, in turn, accelerated development of the precancerous lesions [ 69 ].…”

Section: Immunological Treatment Approaches For Premalignant Lesionsmentioning

confidence: 99%

Redirecting the focus of cancer immunotherapy to premalignant conditions

Young

2017

Cancer Letters

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Much progress has been made in introducing immunological treatment approaches for cancer, with lessons learned from both the successes and failures of immunotherapy. Among the challenges of immunotherapeutic approaches for cancer are the multitudes of mechanisms by which cancers are known to subvert the immune defenses. This has led to the incorporation into the immunotherapeutic arsenal strategies by which to overcome the cancer’s immunological blockades. What has been only superficially explored is the immunological milieu of premalignant lesions and the possibility of immunological approaches for the treatment of premalignant lesions so as to prevent secondary premalignant lesions and their progression to cancer. This review discusses the immunological environment associated with premalignant lesions, and the possible missed opportunity of utilizing immunological treatment strategies in the less hostile environment of premalignant lesions as compared to the immune subversive cancer environment.

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“…Elevated COX-2 expression has been found in most CRC cancer tissues and it is associated with poor prognosis (34)(35)(36)(37). Large epidemiological studies have demonstrated that NSAIDs reduce the risk of CRC cancer in humans and, recently, also an antitumoral activity of NSAIDs has been described in CRC (38)(39)(40).…”

Section: Introductionmentioning

confidence: 99%

Oleocanthal exerts antitumor effects on human liver and colon cancer cells through ROS generation

Cusimano

Balasus

Azzolina

et al. 2017

International Journal of Oncology

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The beneficial health properties of the Mediter-ranean diet are well recognized. The principle source of fat in Mediterranean diet is extra-virgin olive oil (EVOO). Oleocanthal (OC) is a naturally occurring minor phenolic compound isolated from EVOO, which has shown a potent anti-inflammatory activity, by means of its ability to inhibit the cyclooxygenase (COX) enzymes COX-1 and COX-2. A large body of evidence indicates that phenols exhibit anticancer activities. The aim of the present study was to evaluate the potential anticancer effects of OC in hepatocellular carcinoma (HCC) and colorectal carcinoma (CRC) models. A panel of human HCC (HepG2, Huh7, Hep3B and PLC/PRF/5) and CRC (HT29, SW480) cell lines was used. Cells were treated with OC, and cell viability and apoptosis were evaluated. Compared with classical commercially available COX inhibitors (ibuprofen, indomethacin, nimesulide), OC was more effective in inducing cell growth inhibition in HCC and CRC cells. Moreover, OC inhibited colony formation and induced apoptosis, as confirmed by PARP cleavage, activation of caspases 3/7 and chromatin condensation. OC treatment in a dose dependent-manner induced expression of γH2AX, a marker of DNA damage, increased intracellular ROS production and caused mitochondrial depolarization. Moreover, the effects of OC were suppressed by the ROS scavenger N-acetyl-L-cysteine. Finally, OC was not toxic in primary normal human hepatocytes. In conclusion, OC treatment was found to exert a potent anticancer activity against HCC and CRC cells. Taken together, our findings provide preclinical support of the chemotherapeutic potential of EVOO against cancer.

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Chemopreventive action of non-steroidal anti-inflammatory drugs on the inflammatory pathways in colon cancer

Cited by 35 publications

References 45 publications

Evidence for the Involvement of the Master Transcription Factor NF-κB in Cancer Initiation and Progression

Evidence for the Involvement of the Master Transcription Factor NF-κB in Cancer Initiation and Progression

Redirecting the focus of cancer immunotherapy to premalignant conditions

Oleocanthal exerts antitumor effects on human liver and colon cancer cells through ROS generation

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