Background: Curcumin (Cur) is a natural phytochemical that is expected to become an indispensable drug for the treatment of colorectal cancer. A comprehensive understanding of the anti-tumor mechanism of Cur will provide a better reference for its clinical application. This study aimed to examine the effects of extracellular vesicles (EVs) isolated from Cur-medium on RKO colorectal cancer cell proliferation, apoptosis, and migration.
Methods: RKO cells were cultured in various concentrations of Cur-medium, and the EVs were isolated from the Cur-medium. The EVs were identified by transmission electron microscopy and western blotting. The effects of the EVs on RKO cell proliferation, apoptosis, and migration were analyzed, as was the expression of proliferating cell nuclear antigen (PCNA), Bax, vimentin, and E-cadherin. The expression of nuclear factor κB (NF-κB) p65 in the EVs was also detected.
Results: Our results showed that the EVs isolated from the Cur-medium weakened RKO cell proliferation and migration but had no effect on cell apoptosis. Cur suppressed the expression of NF-κB p65 in the EVs. Overall, this study revealed that Cur exerts anti-tumor effects by suppressing NF-κB p65 in EVs to weaken RKO cell proliferation and migration.
Conclusions: In conclusion, the packaging of Cur into EVs is expected to become an indispensable treatment of colorectal cancer in the future.
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http://dx.doi.org/10.21037/tcr-24-98 | DOI Listing |
J Biomater Appl
March 2025
Department of Chemistry, School of Pharmacy, North Sichuan Medical College, Nanchong, China.
Colorectal cancer is the fourth leading cause of cancer-related deaths worldwide. Capecitabine is a chemotherapeutic agent commonly used for the treatment of colon cancer. To realize local sustained release, promote efficient local intracellular transport, and mitigate the systemic toxic effects of capecitabine, a capecitabine prodrug, capecitabine-poly (p-dioxanone) (Cap-PPDO), was successfully synthesized.
View Article and Find Full Text PDFInvest Ophthalmol Vis Sci
March 2025
Department of Bioengineering, University of Texas at Dallas, Richardson, Texas, United States.
Purpose: After stromal injury to the cornea, the release of growth factors and pro-inflammatory cytokines promotes the activation of quiescent keratocytes into a migratory fibroblast and/or fibrotic myofibroblast phenotype. Persistence of the myofibroblast phenotype can lead to corneal fibrosis and scarring, which are leading causes of blindness worldwide. This study aims to establish comprehensive transcriptional profiles for cultured corneal keratocytes, fibroblasts, and myofibroblasts to gain insights into the mechanisms through which these phenotypic changes occur.
View Article and Find Full Text PDFJ Exp Med
June 2025
Department of Pathology, New York University Grossman School of Medicine, New York, NY, USA.
Leukemia-driving mutations are thought to arise in hematopoietic stem cells (HSC), yet the natural history of their spread is poorly understood. We genetically induced mutations within endogenous murine HSC and traced them in unmanipulated animals. In contrast to mutations associated with clonal hematopoiesis (such as Tet2 deletion), the leukemogenic KrasG12D mutation dramatically accelerated HSC contribution to all hematopoietic lineages.
View Article and Find Full Text PDFMed Res Rev
March 2025
Biochemistry and Molecular Biology, Primeasia University, Banani, Dhaka, Bangladesh.
The development of standard drugs for some unusual cancers, including estrogen-nonresponsive breast cancer, is somewhat difficult within a very short time. So, considering the current situation, phytoestrogen may be a potential candidate for unraveling chemotherapeutics agents. The reason for this review article is to manifest overall information regarding the effects of phytoestrogen on triple-negative breast cancer (TNBC), along with its related cellular and molecular pathways in different TNBC models.
View Article and Find Full Text PDFCytoskeleton (Hoboken)
March 2025
Biology Department, Mount Saint Vincent University, Halifax, Canada.
The organization of microtubules into a mitotic spindle is critical for animal cell proliferation and involves the cooperation of hundreds of proteins whose molecular roles and regulation are not fully understood. The protein product of the Drosophila gene abnormal spindle, Asp, is a microtubule-associated protein required for correct mitotic spindle formation. To better understand the contribution of Asp to microtubule organization during spindle formation, we reverse-engineered flies to express a version of Asp (Asp), predicted to have lost its ability to bind the phosphatase trimer PP2A-B56.
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