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Novel therapeutic agents to combat cancer is an active area of research, as current treatment options have limitations in efficacy and tolerability. One of these therapeutic agents in our immediate environment is cyclolinopeptides (CLPs). CLPs have several advantages that make them suitable for daily consumption and potential therapeutics in cancer research. They are natural compounds, having high specificity, low toxicity, low cost, and an overall simple extraction process. Over the years, numerous in vitro studies in cancer cells demonstrated CLPs to possess anti-proliferative, apoptotic, and anti-angiogenic effects, as well as the ability to induce cell cycle arrest and inhibit cancer cell growth in various cancer types, including breast cancer, gastric cancer, and melanoma. This paper provides an overview of the significance and potential of CLPs as therapeutic agents, emphasizing their promising role in cancer treatment based on different cancer cell lines. The mechanism of action of CLPs in cancer cells is multifaceted. It involves the modulation of multiple signaling pathways, including inhibition of protein kinases, modulation of apoptosis-related proteins, and regulation of oxidative stress and inflammation.
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http://dx.doi.org/10.3390/cancers15153874 | DOI Listing |
Fundam Clin Pharmacol
October 2025
Postgraduate Program in Pharmaceutical Science, Federal University of Juiz de Fora, Juiz de Fora, Minas Gerais, Brazil.
This review highlights the integration of drug repurposing and nanotechnology-driven delivery strategies as innovative approaches to enhance the antifungal activity of statins against mucosal candidiasis, providing a framework for future translational research and clinical application. The rising prevalence of antifungal resistance and virulence factors of Candida albicans underscore the limitations of current therapies. Statins, commonly used as lipid-lowering agents, have emerged as attractive repurposed drug candidates due to their ability to interfere with fungal ergosterol biosynthesis and Ras-mediated signaling pathways.
View Article and Find Full Text PDFMol Biotechnol
September 2025
Department of Biology, Faculty of Science, Marmara University, Göztepe, 34722, Istanbul, Türkiye.
Babesia bigemina, a tick-borne protozoan parasite, is one of the main causative agents of bovine babesiosis, a disease with significant economic impact on the cattle industry. One of the key enzymes involved in the parasite's metabolism is lactate dehydrogenase (LDH), which plays an essential role in the anaerobic glycolytic pathway by catalysing the conversion of pyruvate to lactate. In this study, B.
View Article and Find Full Text PDFNat Biotechnol
September 2025
Key Laboratory of RNA Innovation, Science and Engineering, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, China.
Targeted protein degraders hold potential as therapeutic agents to target conventionally 'undruggable' proteins. Here, we develop a high-throughput screen, DEath FUSion Escaper (DEFUSE), to identify small-molecule protein degraders. By conjugating the protein of interest to a fast-acting triggerable death protein, this approach translates target protein degradation into a cell survival phenotype to illustrate the presence of degraders.
View Article and Find Full Text PDFNat Rev Urol
September 2025
Department of Genitourinary Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
Low-grade non-muscle invasive bladder cancer is a specific category of bladder cancer with a favourable prognosis; however, its management presents several challenges. The risk of stage progression is very low, but approximately half of patients will experience recurrence within the first 5 years after diagnosis. This high propensity for recurrence, coupled with the threat of progression, mandates ongoing surveillance.
View Article and Find Full Text PDFNat Commun
September 2025
Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA.
With the approval of the antibody-drug conjugate enfortumab vedotin (EV), NECTIN4 has emerged as a bona fide therapeutic target in urothelial carcinoma (UC). Here, we report the development of a NECTIN4-directed chimeric antigen receptor (CAR) T cell, which exhibits reactivity across cells expressing a range of endogenous NECTIN4, with enhanced activity in high expressors. We demonstrate that the PPARγ pathway, critical for luminal differentiation, transcriptionally controls NECTIN4, and that the PPARγ agonist rosiglitazone primes and augments NECTIN4 expression, thereby increasing sensitivity to NECTIN4-CAR T cell-mediated killing.
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