This study aimed to investigate the effect of AOPPs on apoptosis in human chondrocytes. Chondrocytes were treated with AOPPs. Cell death, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, reactive oxygen species (ROS) generation, and the expression of apoptotic proteins were detected in vitro. AOPPs levels were detected by colorimetric method. The results in vitro demonstrated that AOPPs induced cell death in human chondrocyte through a redox-dependent pathway, including RAGE-mediated, NADPH oxidase-dependent ROS generation, and poly (ADP-ribose) polymerase-1 (PARP-1) activation. Targeting AOPPs-induced cellular mechanisms might emerge as a promising therapeutic option for patients with RA.
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http://dx.doi.org/10.1007/s10495-016-1314-6 | DOI Listing |
Iran J Med Sci
December 2024
Department of Biology, Faculty of Science and Technology, Universitas Airlangga, Surabaya, Indonesia.
Background: In approximately 80% of colorectal cancer cases, mutations in the adenomatous polyposis coli () gene disrupt the Wingless-related integration site (Wnt)/β-catenin signaling pathway, a crucial factor in carcinogenesis. This disruption may result in consequences such as aberrant spindle segregation and mitotic catastrophe. This study aimed to analyze the effectiveness of the ethanolic extract of red okra () pods (EEROP) in inducing apoptosis in colorectal cancer cells (SW480) by inhibiting the Wnt/β-catenin signaling pathway.
View Article and Find Full Text PDFNat Cancer
January 2025
Department of Molecular, Cell, and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Tumors lacking the BRCA1 and BRCA2 (BRCA) hereditary breast cancer genes display heightened sensitivity to anti-cancer treatments, such as inhibitors of poly (ADP-ribose) polymerase 1 (PARP1). However, when resistance develops, treatments are lacking. Using CRISPR technology, we discovered that enhancing homologous recombination through increased DNA end resection in BRCA1-deficient cells by loss of the 53BP1-Shieldin complex-which is associated with resistance to PARP inhibitors-also heightens sensitivity to DNA nicks.
View Article and Find Full Text PDFBiochim Biophys Acta Mol Basis Dis
January 2025
Department of Organ Transplantation, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei, PR China; Department of Urology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei, PR China. Electronic address:
Background: Renal ischemia-reperfusion injury (RIRI) stands as an unavoidable complication arising from kidney surgery, profoundly intertwined with its prognosis. The role of differentially expressed in FDCP 6 homolog (DEF6) in RIRI remains elusive, despite its confirmation as a potential therapeutic target for diverse diseases. Here, we investigated the mechanism by which DEF6 regulated RIRI.
View Article and Find Full Text PDFInt J Hyperthermia
December 2025
Laboratory for Experimental Oncology and Radiobiology (LEXOR), Amsterdam University Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Efficacy of current treatment options for cervical cancer require improvement. Previous studies have shown the enhancing effects of the addition of PARP1-inhibitors to chemoradiotherapy and thermoradiotherapy. The aim of our present study was to test efficacy of different combinations of treatment modalities radiotherapy, cisplatin, hyperthermia and PARP1-inhibitors using tumor models, treated patient samples and tumor models.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Triple-negative breast cancer (TNBC) is a difficulty and bottleneck in the clinical treatment of breast cancer due to a lack of effective therapeutic targets. Herein, we first report that secernin 2 (SCRN2), an uncharacterized gene in human cancer, acts as a novel tumor suppressor in TNBC to inhibit cancer progression and enhance therapeutic sensitivity to poly(ADP-ribose) polymerase (PARP) inhibition both in vitro and in vivo. SCRN2 is downregulated in TNBC through chaperone-mediated autophagic degradation, and its downregulation is associated with poor patient prognosis.
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