Tag: Cancer research

The ubiquitin–proteasome system (UPS) regulates protein turnover and controls cell‑cycle progression, DNA repair, apoptosis and oncogenic signalling. In cancer, UPS components become dysregulated, leading to excessive degradation of tumour suppressors and stabilisation of oncogenic proteins. This imbalance drives tumour growth and makes UPS a powerful therapeutic target.

The G1/S transition is the critical checkpoint where a cell commits to DNA replication. It integrates cyclin–CDK activity, Rb phosphorylation, and E2F activation to ensure accurate S‑phase entry. Proper regulation protects genomic stability and prevents uncontrolled proliferation.

Cancer is a multifaceted disease caused by the uncontrolled growth of abnormal cells. It develops through genetic and epigenetic alterations, environmental exposures, and interactions within the tumour microenvironment. Understanding these processes is essential for improving prevention, diagnosis, and treatment.

The autophagy-lysosome pathway is the cell’s primary degradation and recycling system, responsible for clearing damaged proteins, dysfunctional organelles, and intracellular pathogens. Dysfunction in this pathway has been linked to neurodegenerative disorders, cancer, and metabolic syndromes. This article explores how the process works, its role in disease prevention, and emerging therapeutic strategies targeting this vital cellular mechanism.

Cell‑cycle and proliferation study tools provide essential insights into how cells grow and divide. Techniques such as BrdU and EdU incorporation, flow‑cytometric DNA content analysis, Ki‑67 and phospho‑H3 staining, FUCCI reporters and genetic manipulation allow researchers to measure cell‑cycle phases, DNA synthesis and mitotic activity with high precision.