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Homologous recombination promotes non-immunogenic mitotic cell death upon DNA damage.
Nat Cell Biol
January 2025
Genome Integrity Unit, Children's Medical Research Institute, University of Sydney, Westmead, New South Wales, Australia.
Double-strand breaks (DSBs) can initiate mitotic catastrophe, a complex oncosuppressive phenomenon characterized by cell death during or after cell division. Here we unveil how cell cycle-regulated DSB repair guides disparate cell death outcomes through single-cell analysis of extended live imaging. Following DSB induction in S or G2, passage of unresolved homologous recombination intermediates into mitosis promotes non-immunogenic intrinsic apoptosis in the immediate attempt at cell division.
View Article and Find Full Text PDFThe role of inflammasomes in hepatocellular carcinoma: Mechanisms and therapeutic insights.
Ann Hepatol
December 2024
Scientific Direction, National Institute of Gastroenterology, "S. de Bellis", IRCCS Research Hospital, Via Turi 27, Castellana Grotte, 70013 Bari, Italy. Electronic address:
Hepatocellular carcinoma is among the most frequent forms of primary liver cancer and develops within a context of chronic inflammation, frequently associated with a multitude of risk factors, including viral infections, metabolic dysfunction-associated fatty liver disease, metabolic dysfunction-associated steatohepatitis and liver fibrosis. The tumor microenvironment is crucial for the progression of HCC, as immune cells, tumor-associated fibroblasts and hepatic stellate cells interact to promote chronic inflammation and tumor spread. Inflammasomes, the multiprotein complexes that launch the innate immune response, emerge as important mediators in the pathogenesis of HCC.
View Article and Find Full Text PDFTENT5A mediates the cancer-inhibiting effects of EGR1 by suppressing the protein stability of RPL35 in hepatocellular carcinoma.
Cell Oncol (Dordr)
December 2024
State Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, 25/Ln 2200 Xietu Road, Shanghai, 200032, China.
Purpose: Terminal nucleotidyltransferase 5A (TENT5A), recently predicted as a non-canonical poly(A) polymerase, is critically involved in several human disorders including retinitis pigmentosa, cancer and obesity. However, the exact biological role of TENT5A in hepatocellular carcinoma (HCC) has not been elucidated.
Methods: The transcription level of TENT5A and clinical correlation were analyzed using the LIRI-JP cohort, the TCGA-LIHC cohort, and clinical tissue samples of HCC patients in our laboratory.
miR-128-3p suppresses tumor growth and enhances chemosensitivity in tongue squamous cell carcinoma through MAP2K7 targeting.
Mol Biol Rep
October 2024
RNAi and Functional Genomics Lab, Department of Life Science, National Institute of Technology Rourkela, Rourkela, Odisha, 769008, India.
Background: MicroRNAs (miRNAs), which are key players in cancer cell resistance to chemotherapy, notably target genes associated with drug resistance. While miRNA-128-3p is recognized for its involvement in various cancers, its specific role in tumorigenesis and cisplatin (CIS) resistance in tongue cancer remains unclear. Therefore, in the present study, we endeavoured to elucidate the significance of miR-128-3p in tongue squamous cell carcinoma (TSCC), shedding light on its intricate functions and underlying mechanisms.
View Article and Find Full Text PDFRational design, synthesis, and biophysical characterization of a peptidic MDM2-MDM4 interaction inhibitor.
Bioorg Med Chem
November 2024
Dipartimento di Scienze Farmaceutiche, Università degli Studi di Perugia, Via del Liceo, 1, 06123 Perugia, Italy. Electronic address:
In recent years, the restoration of p53 physiological functions has become an attractive therapeutic approach to develop novel and efficacious cancer therapies. Among other mechanisms, the oncosuppressor protein p53 is functionally regulated by MDM2 through its E3 ligase function. MDM2 promotes p53 ubiquitination and degradation following homodimerization or heterodimerization with MDM4.
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