Histological tumor necrosis (TN) has been reported to indicate a poor prognosis for different human cancers. It is generally accepted that TN results from chronic ischemic injury due to rapid tumor growth. However, whether insufficient tumor vascularization and inadequate tumor cell oxygenation are the only factors causing TN remains controversial. Mitotic catastrophe is considered to occur as a result of dysregulated/failed mitosis, leading to cell death. We hypothesize that mitotic catastrophe, induced by hypoxic stress, may lead to the TN which is observed in high grade carcinomas. The current review describes the morphological features of TN in malignant epithelial tumors. In addition, evidence regarding the involvement of mitotic catastrophe in the induction of TN in human carcinomas is discussed.
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http://dx.doi.org/10.3892/ol.2014.2345 | DOI Listing |
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 PDFInt J Biol Sci
January 2025
Department of Biochemistry, School of Medicine, Keimyung University, Daegu 42601, Republic of Korea.
Renal cell carcinoma (RCC) is considered as a "metabolic disease" due to various perturbations in metabolic pathways that could drive cancer development. Glycine decarboxylase (GLDC) is a mitochondrial enzyme that takes part in the oxidation of glycine to support nucleotide biosynthesis via transfer of one-carbon units. Herein, we aimed to investigate the potential role of GLDC in RCC development.
View Article and Find Full Text PDFClin Transl Med
January 2025
Department of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China.
Background: Chromosomal instability (CIN), a hallmark of cancer, is commonly linked to poor prognosis in high-grade prostate cancer (PCa). Paradoxically, excessively high levels of CIN may impair cancer cell viability. Consequently, understanding how tumours adapt to CIN is critical for identifying novel therapeutic targets.
View Article and Find Full Text PDFEMBO J
January 2025
Newcastle University Biosciences Institute (NUBI), Central Parkway, Newcastle University, NE1 3BZ, Newcastle upon Tyne, UK.
The cellular concentrations of splicing factors (SFs) are critical for controlling alternative splicing. Most serine and arginine-enriched (SR) protein SFs regulate their own concentration via a homeostatic feedback mechanism that involves regulation of inclusion of non-coding 'poison exons' (PEs) that target transcripts for nonsense-mediated decay. The importance of SR protein PE splicing during animal development is largely unknown despite PE ultra-conservation across animal genomes.
View Article and Find Full Text PDFBMC Cancer
December 2024
Department of Gynecology, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Peking University Cancer Hospital Yunnan, Kunming, 650118, Yunnan, P. R. China.
New treatment strategies for ovarian cancer, which is the deadliest female reproductive tract malignancy, are urgently needed. Here, we investigated the anticancer effects of fenbendazole (FBZ), a benzimidazole compound, on the regulation of apoptosis and mitotic catastrophe in A2780 and SKOV3 human epithelial ovarian cancer cells. Functional experiments, including Cell Counting Kit 8 (CCK-8), colony formation, and flow cytometry assays, were conducted to explore the effects of FBZ on the malignant biological behavior of A2780 and SKOV3 cells.
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