Nimesulide inhibits IFN-γ-induced programmed death-1-ligand 1 surface expression in breast cancer cells by COX-2 and PGE2 independent mechanisms

Liang, Mei; Hui, Yang; Fu, Jing

doi:10.1016/j.canlet.2008.10.028

Cited by 40 publications

(26 citation statements)

References 18 publications

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“…In addition, a new class of chemotherapeutic agents, namely nimesulide, has recently been described. Nimesulide is a selective COX-2 inhibitor that has been shown to inhibit IFN-ginduced B7-H1 expression on the surface of breast cancer cells, independently of COX-2/prostaglandin E2 (PGE2) signaling, and to induce cancer cell apoptosis as well as inhibit cancer cell proliferation [86].…”

Section: The Critical Role Of B7-h1 + And/or Pd-1 + Tumor-infiltratinmentioning

confidence: 99%

“…Another strategy to specifically suppress tumor cell activity without affecting T cell function is to inhibit the PI-3-K/mTOR pathway by the use of Honokiol [102]. Moreover, nimesulide can be used to inhibit IFN-g-induced B7-H1 expression on the surface of breast cancer cells, and to induce cancer cell apoptosis as well as inhibition of cancer cell proliferation [86].…”

Section: Expert Opinionmentioning

confidence: 99%

“…Triptolide [103] can be used to decrease B7-H1 expression (7) and Honokiol [102] can be used to block cell proliferation, which does not impair proinflammatory T cell function (8). Finally, nimesulide [86] can also be utilized to inhibit B7-H1 expression, to induce apoptosis and inhibition of cancer cell proliferation (9). The first paper to correlate B7-H1 expression with high proliferative tumour cells.…”

Section: Expert Opinionmentioning

confidence: 99%

See 2 more Smart Citations

Therapeutic targeting of B7-H1 in breast cancer

Hasan

Ghebeh

Lehé

et al. 2011

Expert Opinion on Therapeutic Targets

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B7-H1 should be considered as a potential therapeutic target for breast cancer. Indeed, there is increasing evidence for the potential efficacy of B7-H1 blockade in the prevention of immune evasion by cancer cells. Additionally, B7-H1 targeting can be used in conjunction with other therapeutic modalities for improved efficacy and reduced toxicity. We expect that B7-H1 blockade in combination with other therapeutics will be a prime therapeutic strategy in the future.

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Section: The Critical Role Of B7-h1 + And/or Pd-1 + Tumor-infiltratinmentioning

confidence: 99%

Section: Expert Opinionmentioning

confidence: 99%

Section: Expert Opinionmentioning

confidence: 99%

See 1 more Smart Citation

Therapeutic targeting of B7-H1 in breast cancer

Hasan

Ghebeh

Lehé

et al. 2011

Expert Opinion on Therapeutic Targets

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“…PD-L2 is mainly regulated by cytokines such as IL-10, IL4 and INF-γ (Rodriguez-Garcia et al, 2011;Stanciu et al, 2006). Apparently, IFN-γ is also one of the main regulators of PD-L1 expression in a wide range of cell types (Berthon et al, 2010;Chen et al, 2012;Gong et al, 2009;Liang et al, 2009). Further investigation on the mechanisms of PD-1, PD-L1 and PD-L2 expression and regulation is required to understand the role of these molecules in pathological processes.…”

Section: Expression Of Pd-1 and Its Ligandsmentioning

confidence: 99%

Co-Inhibitory Molecule Programmed Death-1 and Its Ligands: A New Alternative Therapy for Human Immunodeficiency Virus Infection?

Leon-Flores¹

2012

American Journal of Infectious Diseases

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Chronic viral infections are characterized by the up-regulation of a set of immunomodulatory receptors. The over-expression of co-inhibitory molecules on T cells leads to a dysfunctional T cell response with an "exhausted" phenotype. Programmed Death-1 (PD-1) is a molecule that exerts an inhibitory signal on the T cell receptor when it binds to the PD-L1 or PD-L2 ligands present on antigen-presenting cells. Also, the expression of these molecules has been associated to the loss of T cell functions as well as clinical markers of the progression of HIV infection. The study of these molecules has gained attention due to reports indicating that blockade of PD-1 pathway could partially reconstitute T cell functions. In fact, this mechanism has been proposed as an alternative treatment for some chronic viral infections such as HIV infection. This review is focused on those mechanisms that might be favouring the over-expression of PD-1 and its ligands during HIV infection and on the possible new approaches that, by reducing its expression, might represent new strategies for the treatment of HIV infection. Knowing the exact mechanism leading to PD-1, PD-L1 and PDL2 expression in physiologic and pathological conditions is essential for the development of successful treatments. Novel molecular mechanisms inhibiting PD-1 activation might have potential therapeutic use not only in HIV infection but also in other diseases.

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“…It also unveils activity against the rat tongue carcinogenesis which is actually the post-initiation development of squamous cell carcinomas induced by 4-nitroquinoline-1-oxide (Kawamori et al, 2002;Nakatsugi et al, 2000;Yamamoto et al, 2003).In addition, in the case of N-nitrosobis(2-oxopropyl)amine-induced pancreatic tumors in hamster, nimesulide is shown to protect the cells against N-nitrosobis(2-oxopropyl)amine (Furukawa et al, 2003). Nimesulide, in some of the in vitro experiments, is able to inhibit the cell proliferation as well as to increase the rate of apoptosis in various types of cancerous cells (Han and Roman, 2006;Tian et al, 2002;Pan et al, 2003;Li et al, 2003;Liang et al, 2009;Nam et al, 2004;Hida et al, 2000;Eibl et al, 2003). Therefore, it is suggested by the abovementioned fact that inhibition of cancer cell growth is done by nimesulide as well as it also does apoptosis of cancer cells in COX-2-independent manner.…”

Section: Introductionmentioning

confidence: 99%

Atom-based QSAR and 3D QSAR using pharmacophore based alignment for discovery of nimesulide-derived SKBR-3 cell line inhibitors

Choudhury

2014

Med Chem Res

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Growth suppression of many non-COX-2 expressing tumor cells can be exhibited by COX-2 inhibitors, where supplementation of cells with exogenous prostaglandins fails to rescue the cells from growth inhibition. It can, therefore, be speculated that anti-cancer properties of some COX-2 inhibitors may be contributed by the COX-2-independent effects also. Some of the derivatives obtained from certain COX-2 inhibitors which show non-COX-2 inhibitory mechanism have revealed some significant anti-cancer activities. From a COX-2 selective inhibitor nimesulide, an analog JCC76 is derived which is a non-COX-2 active compound and shows inhibition of SKBR-3 breast cancer cell growth. Other JCC76 derived inhibitors also played significant role in SKBR-3 cell inhibition. An analog-based study was done using pharmacophore modeling and 3D-QSAR to provide clues for potential lead compound designing. A five point pharmacophore ADHRR was generated using 39 JCC76-derived SKBR-3 inhibitors. The validated pharmacophore alignment was used for further 3D-QSAR analysis, which presented a good R 2 value of 0.562, 0.982, and 0.848 for atombased QSAR, CoMFA, and CoMSIA model, respectively. All the QSAR models presented good statistical significance and predictivity. The corresponding Q 2 values for each model are 0.513, 0.649, and 0.518, respectively. Both the pharmacophore and CoMSIA results displayed that the H-bond donor and acceptor sites are the key structural feature for JCC76-derived non-COX-2-dependent inhibitors with high activity.

show abstract

Nimesulide inhibits IFN-γ-induced programmed death-1-ligand 1 surface expression in breast cancer cells by COX-2 and PGE2 independent mechanisms

Cited by 40 publications

References 18 publications

Therapeutic targeting of B7-H1 in breast cancer

Therapeutic targeting of B7-H1 in breast cancer

Co-Inhibitory Molecule Programmed Death-1 and Its Ligands: A New Alternative Therapy for Human Immunodeficiency Virus Infection?

Atom-based QSAR and 3D QSAR using pharmacophore based alignment for discovery of nimesulide-derived SKBR-3 cell line inhibitors

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