
Biology, Journal Year: 2024, Volume and Issue: 13(6), P. 425 - 425
Published: June 8, 2024
Tumor cells display abnormal growth and division, avoiding the natural process of cell death. These can be benign (non-cancerous growth) or malignant (cancerous growth). Over past few decades, numerous in vitro vivo tumor models have been employed to understand molecular mechanisms associated with tumorigenesis diverse regards. However, our comprehension how non-tumor transform into at cellular levels remains incomplete. The nematode C. elegans has emerged as an excellent model organism for exploring various phenomena, including tumorigenesis. Although does not naturally develop cancer, it serves a valuable platform identifying oncogenes underlying within live organism. In this review, we describe three distinct germline elegans, highlighting their related regulators: (1) ectopic proliferation due aberrant activation GLP-1/Notch signaling, (2) meiotic entry failure resulting from loss GLD-1/STAR RNA-binding protein, (3) spermatogenic dedifferentiation caused by PUF-8/PUF protein. Each requires mutations specific genes (glp-1, gld-1, puf-8) operates through mechanisms. Despite these differences origins tumorigenesis, internal regulatory networks each shared features. Given conservation many regulators implicated is proposed that unique hold significant potential enhancing broader control governing
Language: Английский