Contribution of non-steroidal anti-inflammatory drugs to breast cancer treatment: In vitro and in vivo studies

abstract

Chronic inflammation plays a crucial role in carcinogenesis. High levels of serum prostaglandin E2 and tissue overexpression of cyclooxygenase-2 (COX -2) have been described in breast, urinary, colorectal, prostate, and lung cancers as being involved in tumor initiation, promotion, progression, angiogenesis, and immunosuppression. Nonsteroidal anti-inflammatory drugs (NSAIDs) are prescribed for several medical conditions to not only decrease pain and fever but also reduce inflammation by inhibiting COX and its product synthesis. To date, significant efforts have been made to better understand and clarify the interplay between cancer development, inflammation, and NSAIDs with a view toward addressing their potential for cancer management. This review provides readers with an overview of the potential use of NSAIDs and selective COX -2 inhibitors for breast cancer treatment, highlighting pre -clinical in vitro and in vivo studies employed to evaluate the efficacy of NSAIDs and their use in combination with other antineoplastic drugs.

keywords

HORMONE-RECEPTOR STATUS; CARCINOMA CELL-LINE; CYCLOOXYGENASE-2 INHIBITOR; MAMMARY-TUMORS; COX-2 INHIBITORS; ANIMAL-MODELS; NSAID USE; HIGH-FAT; CELECOXIB; EXPRESSION

subject category

Agriculture; Veterinary Sciences

authors

Ferreira, T; Faustino-Rocha, AI; Gaspar, VM; Medeiros, R; Mano, JF; Oliveira, PA

our authors

acknowledgements

This work was supported by National Funds from the FCT-Portuguese Foundation for Science and Technology, under the project UIDB/04033/2020 (CITAB) (https://doi.org/10.54499/UIDB/04033/2020) and LA/P/0126/2020 (INOV4AGRO) and through a DoctoralGrant (2020.04789.BD, TiagoFerreira; https://doi.org/10.54499/2020.04789.BD) . This work was also developed within the scope of the project CICECO-Aveiro Institute of Materials, UIDB/50011/2020, UIDP/50011/2020, and LA/P/0006/2020, financed by national funds through the FCT/MEC (PIDDAC) .

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