Purpose: Aspirin, one of the most commonly used nonsteroidal anti-inflammatory drugs (NAIDS), not only shows cancer chemoprevention effects but also improves cancer therapeutic effects when combined with other therapies. Studies that focus on aspirin regulation of the hallmarks of cancer and the associated molecular mechanisms facilitate a more thorough understanding of aspirin in mediating chemoprevention and may supply additional information for the development of novel cancer therapeutic agents.
Methods: The relevant literatures from PubMed have been reviewed in this article.
Results: Current studies have revealed that aspirin regulates almost all the hallmarks of cancer. Within tumor tissue, aspirin suppresses the bioactivities of cancer cells themselves and deteriorates the tumor microenvironment that supports cancer progression. In addition to tumor tissues, blocking of platelet activation also contributes to the ability of aspirin to inhibit cancer progression. In terms of the molecular mechanism, aspirin targets oncogenes and cancer-related signaling pathways and activates certain tumor suppressors.
Conclusion: Beyond a chemopreventive agent, aspirin is a master regulator of the hallmarks of cancer.
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http://dx.doi.org/10.1007/s00432-019-02902-6 | DOI Listing |
Clin Exp Med
January 2025
Department of Thoracic Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
Introduction Recently, immune cells within the tumor microenvironment (TME) have become crucial in regulating cancer progression and treatment responses. The dynamic interactions between tumors and immune cells are emerging as a promising strategy to activate the host's immune system against various cancers. The development and progression of hepatocellular carcinoma (HCC) involve complex biological processes, with the role of the TME and tumor phenotypes still not fully understood.
View Article and Find Full Text PDFSLAS Discov
January 2025
The Hormel Institute, University of Minnesota, Austin, MN 55912. Electronic address:
Metabolic reprogramming of purine biosynthesis is a hallmark of cancer metabolism and represents a critical vulnerability. The enzyme phosphoribosylformylglycinamidine synthase (PFAS) catalyzes the fourth step in de novo purine biosynthesis and has been demonstrated to be prognostic for survival of liver cancer. Despite the importance of this protein as a drug target, there are no known specific inhibitors of PFAS activity.
View Article and Find Full Text PDFBiochem Biophys Res Commun
January 2025
Membranology Unit, Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha, Onna, Okinawa, 904-0495, Japan. Electronic address:
Cellular senescence is an essentially irreversible cell cycle arrest associated with upregulated inflammatory responses that contribute to various pathological and physiological processes, including aging, cancer, and cancer prevention. However, the underlying mechanisms are not fully understood. Here, we show that the downregulation of CNOT3, a subunit of the CCR4-NOT complex that deadenylates mRNA poly(A) tails, promotes cellular senescence in subpopulation of A549 human non-small cell lung cancer cells.
View Article and Find Full Text PDFOncogene
January 2025
Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA.
The functional activation of the androgen receptor (AR) and its interplay with the aberrant Hh/Gli cascade are pivotal in the progression of castration-resistant prostate cancer (CRPC) and resistance to AR-targeted therapies. Our study unveiled a novel role of the truncated form of Gli (t-Gli3) in advancing CRPC. Investigation into Gli3 regulation revealed a Smo-independent mechanism for its activation.
View Article and Find Full Text PDFAdv Exp Med Biol
January 2025
Department of Molecular Biology, Princeton University, Princeton, NJ, USA.
Recent evidence has revealed that cancer is not solely driven by genetic abnormalities but also by significant metabolic dysregulation. Cancer cells exhibit altered metabolic demands and rewiring of cellular metabolism to sustain their malignant characteristics. Metabolic reprogramming has emerged as a hallmark of cancer, playing a complex role in breast cancer initiation, progression, and metastasis.
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